wikidoc - User contributions [en]

User:Shivam Singla

2023-04-26T11:54:42Z

Shivam Singla: /* Professional Background */

==Shivam Singla==
[[File:Shivam Singla.jpg|thumb|360x360px]]
'''Shivam Singla, M.D'''.

Associate Editor-in-Chief at Wikidoc

Email: docshivam@gmail.com

 

==Current Position==
Associate Editor in Chief at Wikidoc, Under Dr. Gibson, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA,USA.

 
==Professional Background==
Dr. Shivam Singla is a medical graduate from Government Medical College, Patiala, India and is currently working as a clinical research assistant at Wayne State University, MI.

He is working as an Associate Editor in Chief at Wikidoc.org.

 

==Education==
2017- M.B.B.S Degree, Government Medical College, Patiala, India

2018 - ECFMG Certification

2017- MCI Certification

 
==Work Experience==

*Dec 2019 - '''Wayne State University, Detroit, MI, United States'''
**Presently, Dr. Shivam Singla is a research fellow working with Dr. Tina Chopra MD in in the department of infectious disease at Wayne State University.
**He works as Associate Editor -in-Chief for WikiDoc. He is Responsible for contributing original content to WikiDoc and editing existing material as well as "watching" the textbook page to assure the validity and neutrality of materials added.

 

*Aug 2019 - Nov 2019 '''Detroit Medical Center/ Wayne State University, MI, United States.'''
**He has worked as a Chief Extern in the department of cardiology and Assisted Dr. Mahir Elder (Cardiologist) along with team of other cardiologists in the morning rounds along with updating patient notes.
**Also participated actively in doing pt's bed side Echo and Treadmill test.
**Assisted cardiologists in various venous insufficiency treatments and PTCA.

 

*July 2019 - Aug 2019 '''Urgent Care, Mount Sinai Medical Center, NY, United States'''

 

*May 2019 - July 2019 '''Heart and Vascular/ Detroit Medical Center, MI, United States.'''
**Hands- On Externship at Heart and vascular at Detroit medical center in the department of cardiology.
**Morning rounds, management plan and notes work up
**Out patient clinic along with senior cardiologist.
**Observing and assisting vascular procedures, stress test and Exercise ECG Work up

 

*April 2019 - May 2019 '''North Shore Hospital, NY, United States'''
**He worked with a pulmonologist in the department of internal medicine.
**He helped typing the management plan and workup for the patients.
**Helped taking history from Spanish patients also.
**Worked In-Patients and outpatients.

 

*Oct 2018 - Mar 2019 '''Providence Hospital, Washington DC, United States.'''
**He worked as an Intern Year Resident/ Extern for 6 months.
**Actively managed patients in ICU /CCU / Night Floats, On- Floors.
**Participated in Grand rounds on every week.
**Actively participated in case presentation and various conferences and seminars.

 

*Aug 2018 - Sep 2018 Melrose Wakefield Hospital /'''Tuft's Clinical Partner, MA'''
**He observed for a period of 6 months in the department of cardio with Director of Cardiology.
**Assisted in cath- lab and making in patient management plans.
**Presentations and grand rounds.

*

 

*

User:Shivam Singla

2021-05-19T07:44:35Z

Shivam Singla: /* Current Position */

==Shivam Singla==
[[File:Shivam Singla.jpg|thumb|360x360px]]
'''Shivam Singla, M.D'''.

Associate Editor-in-Chief at Wikidoc

Email: docshivam@gmail.com

 
==Current Position==
Associate Editor in Chief at Wikidoc, Under Dr. Gibson, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA,USA.

 
==Professional Background==
Dr. Shivam Singla is a medical graduate from Government Medical College, Patiala, India and is currently working as a clinical research assistant at Wayne State University, MI.

He is working as an Associate Editor in Chief at Wikidoc.org.

 
==Education==
2017- M.B.B.S Degree, Government Medical College, Patiala, India

2018 - ECFMG Certification

2017- MCI Certification

 
==Work Experience==

*Dec 2019 - '''Wayne State University, Detroit, MI, United States'''
**Presently, Dr. Shivam Singla is a research fellow working with Dr. Tina Chopra MD in in the department of infectious disease at Wayne State University.
**He works as Associate Editor -in-Chief for WikiDoc. He is Responsible for contributing original content to WikiDoc and editing existing material as well as "watching" the textbook page to assure the validity and neutrality of materials added.

 

*Aug 2019 - Nov 2019 '''Detroit Medical Center/ Wayne State University, MI, United States.'''
**He has worked as a Chief Extern in the department of cardiology and Assisted Dr. Mahir Elder (Cardiologist) along with team of other cardiologists in the morning rounds along with updating patient notes.
**Also participated actively in doing pt's bed side Echo and Treadmill test.
**Assisted cardiologists in various venous insufficiency treatments and PTCA.

 

*July 2019 - Aug 2019 '''Urgent Care, Mount Sinai Medical Center, NY, United States'''

 

*May 2019 - July 2019 '''Heart and Vascular/ Detroit Medical Center, MI, United States.'''
**Hands- On Externship at Heart and vascular at Detroit medical center in the department of cardiology.
**Morning rounds, management plan and notes work up
**Out patient clinic along with senior cardiologist.
**Observing and assisting vascular procedures, stress test and Exercise ECG Work up

 

*April 2019 - May 2019 '''North Shore Hospital, NY, United States'''
**He worked with a pulmonologist in the department of internal medicine.
**He helped typing the management plan and workup for the patients.
**Helped taking history from Spanish patients also.
**Worked In-Patients and outpatients.

 

*Oct 2018 - Mar 2019 '''Providence Hospital, Washington DC, United States.'''
**He worked as an Intern Year Resident/ Extern for 6 months.
**Actively managed patients in ICU /CCU / Night Floats, On- Floors.
**Participated in Grand rounds on every week.
**Actively participated in case presentation and various conferences and seminars.

 

*Aug 2018 - Sep 2018 Melrose Wakefield Hospital /'''Tuft's Clinical Partner, MA'''
**He observed for a period of 6 months in the department of cardio with Director of Cardiology.
**Assisted in cath- lab and making in patient management plans.
**Presentations and grand rounds.

*

 

*

User:Shivam Singla

2021-05-19T07:43:39Z

Shivam Singla: /* Current Position */

==Shivam Singla==
[[File:Shivam Singla.jpg|thumb|360x360px]]
'''Shivam Singla, M.D'''.

Associate Editor-in-Chief at Wikidoc

Email: docshivam@gmail.com

 
==Current Position==
Associate Editor in Chief at Wikidoc, Under Dr. Gibson, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA,USA.

 
==Professional Background==
Dr. Shivam Singla is a medical graduate from Government Medical College, Patiala, India and is currently working as a clinical research assistant at Wayne State University, MI.

He is working as an Associate Editor in Chief at Wikidoc.org.

 
==Education==
2017- M.B.B.S Degree, Government Medical College, Patiala, India

2018 - ECFMG Certification

2017- MCI Certification

 
==Work Experience==

*Dec 2019 - '''Wayne State University, Detroit, MI, United States'''
**Presently, Dr. Shivam Singla is a research fellow working with Dr. Tina Chopra MD in in the department of infectious disease at Wayne State University.
**He works as Associate Editor -in-Chief for WikiDoc. He is Responsible for contributing original content to WikiDoc and editing existing material as well as "watching" the textbook page to assure the validity and neutrality of materials added.

 

*Aug 2019 - Nov 2019 '''Detroit Medical Center/ Wayne State University, MI, United States.'''
**He has worked as a Chief Extern in the department of cardiology and Assisted Dr. Mahir Elder (Cardiologist) along with team of other cardiologists in the morning rounds along with updating patient notes.
**Also participated actively in doing pt's bed side Echo and Treadmill test.
**Assisted cardiologists in various venous insufficiency treatments and PTCA.

 

*July 2019 - Aug 2019 '''Urgent Care, Mount Sinai Medical Center, NY, United States'''

 

*May 2019 - July 2019 '''Heart and Vascular/ Detroit Medical Center, MI, United States.'''
**Hands- On Externship at Heart and vascular at Detroit medical center in the department of cardiology.
**Morning rounds, management plan and notes work up
**Out patient clinic along with senior cardiologist.
**Observing and assisting vascular procedures, stress test and Exercise ECG Work up

 

*April 2019 - May 2019 '''North Shore Hospital, NY, United States'''
**He worked with a pulmonologist in the department of internal medicine.
**He helped typing the management plan and workup for the patients.
**Helped taking history from Spanish patients also.
**Worked In-Patients and outpatients.

 

*Oct 2018 - Mar 2019 '''Providence Hospital, Washington DC, United States.'''
**He worked as an Intern Year Resident/ Extern for 6 months.
**Actively managed patients in ICU /CCU / Night Floats, On- Floors.
**Participated in Grand rounds on every week.
**Actively participated in case presentation and various conferences and seminars.

 

*Aug 2018 - Sep 2018 Melrose Wakefield Hospital /'''Tuft's Clinical Partner, MA'''
**He observed for a period of 6 months in the department of cardio with Director of Cardiology.
**Assisted in cath- lab and making in patient management plans.
**Presentations and grand rounds.

*

 

*

Renal artery stenosis overview

2021-04-08T07:33:43Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the [[renal arteries]] or their proximal branches of more than 50% in diameter.
*[[Renal artery stenosis|RAS]] is a heterogeneous group of diseases that most commonly include: [[Fibromuscular dysplasia|fibromuscular dysplasia (FMD)]] and [[atherosclerotic]] renal artery stenosis (ARAS).
*Although [[renal artery stenosis]] may be an isolated asymptomatic condition,
*It may commonly lead to [[secondary hypertension]] that is thus called [[renovascular hypertension (RVHT)]], [[ischemic nephropathy]], and [[Chronic renal insufficiency|chronic renal insufficiency.]]

*Approximately 90% of [[renal artery stenosis]] cases occur due to progressive [[atherosclerosis]].
*The ostium and proximal third of the renal arteries are the most commonly involved regions in [[atherosclerosis]].
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of [[chronic kidney disease]] and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind [[renal artery stenosis]] is reduction in renal blood flow
*Secondary to [[renal artery stenosis]] which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor reflex]], and the [[sympathetic nervous system]].

*Elevated angiotensin II activities in turn cause elevation of the [[arterial pressure]] and other effects including [[Aldosterone|aldosterone secretion]], sodium retention, and [[left ventricular hypertrophy]] and remodeling.

==Causes==

*[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic plaque]] in the renal arteries (termed [[atherosclerotic]] renal artery stenosis).
*Less frequently, it is caused by [[fibromuscular dysplasia]].

==Classification==

*[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]].

*Additionally, [[renal artery stenosis]] is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in [[Renal artery stenosis|RAS]]. This classification simply differentiates between hemodynamically insignificant [[Renal artery stenosis]] (< 75% stenosis) and hemodynamically significant [[Renal artery stenosis]] (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic [[renal artery stenosis]] (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with [[cardiovascular]] co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**[[Atherosclerosis]]
**Advanced age
**[[Dyslipidemia]]
**[[Diabetes mellitus]]
**[[Smoking]]
**[[Hypertension]]

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of [[Renal artery stenosis|ARAS]].

*[[Doppler ultrasonography]], [[CTA]], and [[MRA]] may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as [[renal angiography]], is considered the gold standard for diagnosis and may be used when
*Concomitant [[Catheterization|catheterizations]] are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with [[ARAS]].

*Several [[anti-hypertensive]] [[medications]] have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of [[PAD]], [[ACE-I]] and [[CCB]] may be used in [[patients]] with RAS because they have an effect on both lowering BP and delaying the [[renal disease]].

*Other [[blood pressure]]-lowering medications include [[beta-blockers]], [[hydrazine]], and [[chlorothiazide]].

*Although [[ARBs]] may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*[[Angioplasty]] and [[stent]] implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the [[CORAL]] trial showed that although there are high technical success rates with [[angioplasty]]/[[stenting]], the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI ([[percutaneous renal interventions]]) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the [[renal arteries]] may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==Case studies==

==References==

Renal artery stenosis pathophysiology

2021-04-08T07:29:47Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[Juxtaglomerular apparatus|juxtaglomerular apparatu]]<nowiki/>s through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the [[renin-angiotensin-aldosterone system]]<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to [[Angiotensin II]] with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

== Pathogenesis ==
[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the [[rarefaction]] of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes [[irreversible]] and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]].

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis pathophysiology

2021-04-08T07:28:44Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[Juxtaglomerular apparatus|juxtaglomerular apparatu]]<nowiki/>s through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the [[renin-angiotensin-aldosterone system]]<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to [[Angiotensin II]] with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

== Pathogenesis ==
[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the [[rarefaction]] of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]]<ref name="pmid11079647">{{cite journal |vauthors=Herrmann HC, Moliterno DJ, Ohman EM, Stebbins AL, Bode C, Betriu A, Forycki F, Miklin JS, Bachinsky WB, Lincoff AM, Califf RM, Topol EJ |title=Facilitation of early percutaneous coronary intervention after reteplase with or without abciximab in acute myocardial infarction: results from the SPEED (GUSTO-4 Pilot) Trial |journal=J Am Coll Cardiol |volume=36 |issue=5 |pages=1489–96 |date=November 2000 |pmid=11079647 |doi=10.1016/s0735-1097(00)00923-2 |url=}}</ref>.

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis physical examination

2020-12-20T20:17:22Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
A "whooshing" noise ([[bruit]]) can be heard over the abdomen.

Physical examination of patients with [[renal artery stenosis]] is usually normal except for the [[bruit]] that is heard in most of the cases on [[auscultation]]<ref name="urlRenal Artery Stenosis - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK430718/ |title=Renal Artery Stenosis - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref>.

===Appearance of the [[Patient]]===

*General appearance of [[patients]] with [[renal artery stenosis]] appears stable with some discomfort seen in cases due to [[resistant hypertension]].

===[[Vital Signs]]===

*[[High blood pressure]] with [[normal]] [[pulse pressure]], [[tachycardia]].

===[[Skin]]===

*[[Skin]] examination of patients with [[renal artery stenosis]] is usually normal

===HEENT===

*[[HEENT]] examination of patients with [[renal artery stenosis]] is usually normal but in some cases, [[vision]] changes or [[headache]] may be present as a [[complication]] of [[hypertension]].

===Neck===

*[[Neck]] examination of patients with [[renal artery stenosis]] is usually normal

===Lungs===

*[[Pulmonary]] examination of patients with [[renal artery stenosis]] is usually normal but in some cases, there may be the presence of flash [[pulmonary edema]].
*Fine/coarse [[crackles]] upon auscultation of the [[lung]] bases bilaterally

===Heart===

*[[Cardiovascular]] examination of [[patients]] with [[renal artery stenosis]] is usually normal with normal S1, S2, no [[murmurs]], [[gallops]].

===Abdomen===

*[[Abdominal]] examination: The presence of [[bruit]] is a characteristic finding seen in patients with [[renal artery stenosis]]

===Back===

*Back examination of patients with [[renal artery stenosis]] is usually normal.

===Genitourinary===

*[[Genitourinary]] examination of patients with [[renal artery stenosis]] is usually normal.

===Neuromuscular===

*[[Neuromuscular]] examination of patients with [[renal artery stenosis]] is usually normal.

===Extremities===

*Extremities examination of patients with [[renal artery stenosis]] is usually normal.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Renal artery stenosis physical examination

2020-12-20T20:14:34Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
A "whooshing" noise ([[bruit]]) can be heard over the abdomen.

Physical examination of patients with [[renal artery stenosis]] is usually normal except for the [[bruit]] that is heard in most of the cases on [[auscultation]].

===Appearance of the [[Patient]]===

*General appearance of [[patients]] with [[renal artery stenosis]] appears stable with some discomfort seen in cases due to [[resistant hypertension]].

===[[Vital Signs]]===

*[[High blood pressure]] with [[normal]] [[pulse pressure]], [[tachycardia]].

===[[Skin]]===

*[[Skin]] examination of patients with [[renal artery stenosis]] is usually normal

===HEENT===

*[[HEENT]] examination of patients with [[renal artery stenosis]] is usually normal but in some cases, [[vision]] changes or [[headache]] may be present as a [[complication]] of [[hypertension]].

===Neck===

*[[Neck]] examination of patients with [[renal artery stenosis]] is usually normal

===Lungs===

*[[Pulmonary]] examination of patients with [[renal artery stenosis]] is usually normal but in some cases, there may be the presence of flash [[pulmonary edema]].
*Fine/coarse [[crackles]] upon auscultation of the [[lung]] bases bilaterally

===Heart===

*[[Cardiovascular]] examination of [[patients]] with [[renal artery stenosis]] is usually normal with normal S1, S2, no [[murmurs]], [[gallops]].

===Abdomen===

*[[Abdominal]] examination: The presence of [[bruit]] is a characteristic finding seen in patients with [[renal artery stenosis]]

===Back===

*Back examination of patients with [[renal artery stenosis]] is usually normal.

===Genitourinary===

*[[Genitourinary]] examination of patients with [[renal artery stenosis]] is usually normal.

===Neuromuscular===

*[[Neuromuscular]] examination of patients with [[renal artery stenosis]] is usually normal.

===Extremities===

*Extremities examination of patients with [[renal artery stenosis]] is usually normal.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Renal artery stenosis physical examination

2020-12-20T20:09:10Z

Shivam Singla: /* Overview */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}

==Overview==
A "whooshing" noise ([[bruit]]) can be heard over the abdomen.

Physical examination of patients with renal artery stenosis is usually normal except for the bruit that is heard in most of the cases on auscultation.

===Appearance of the Patient===

*General appearance of patients with renal artery stenosis appears stable with some discomfort seen in cases due to the resistant hypertension.

===Vital Signs===

*High blood pressure with normal pulse pressure, tachycardia.

===Skin===

*Skin examination of patients with renal artery stenosis is usually normal

===HEENT===

*HEENT examination of patients with renal artery stenosis is usually normal but in some cases vision changes or headache may be present as a complication of hypertension.

===Neck===

*Neck examination of patients with renal artery stenosis is usually normal

===Lungs===

*Pulmonary examination of patients with renal artery stenosis is usually normal but in some cases there may be the presence of flash pulmonary edema.
*Fine/coarse [[crackles]] upon auscultation of the lung bases bilaterally

===Heart===

*Cardiovascular examination of patients with renal artery stenosis's is usually normal with normal S1,S2, no murmurs, gallops.

===Abdomen===

*Abdominal examination : Presence of bruit is a characteristic finding seen in patients with renal artery stenosis

===Back===

*Back examination of patients with renal artery stenosis is usually normal.

===Genitourinary===

*Genitourinary examination of patients with renal artery stenosis is usually normal.

===Neuromuscular===

*Neuromuscular examination of patients with renal artery stenosis is usually normal.

===Extremities===

*Extremities examination of patients with renal artery stenosis is usually normal.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Renal artery stenosis history and symptoms

2020-12-20T19:41:59Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]]

==Overview==
In a patient suspected to have [[atherosclerosis]], [[Hypertension causes|resistant hypertension]] and a drop in the predicted [[glomerular filtration rate]] (eGFR) are three elements that are very critical for increasing the presumption of atherosclerotic [[renal artery stenosis]]. Other factors, such as [[hypertension]] at an early age or [[malignant hypertension]], play a major role as well.

==History and symptoms==
According to the KDOQI Clinical Practice Guidelines on Hypertension and [[Antihypertensive]] Agents in [[Chronic kidney diseas|Chronic Kidney Disease]]<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>, the most important clinical clues that should raise the suspicion of renal artery disease are the triad:

*Resistant [[Hypertension, systemic|Hypertension]]
*Reduced in estimated [[Glomerular filtration rate|glomerular Filtration rate]] (eGFR)
*Known generalized [[atherosclerosis]]

Additional clinical clues that suggest renal artery disease are listed below<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>:

*Age of [[hypertension]] < 30 years and > 55 years
*Abrupt onset of [[hypertension]]
*Accelerated [[hypertension]] that was previously well-controlled
*Refractory [[hypertension]] to 3 anti-hypertensive medications
*[[Malignant hypertension]]
*[[Smoking]]
*Abdominal bruit
*[[Flash pulmonary edema]]
*Generalized atherosclerosis obliterans
*Asymmetric [[kidney]] sizes
*[[Acute kidney injury]] when ACE-I or ARB are used for treatment

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis history and symptoms

2020-12-20T19:38:45Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]]

==Overview==
Resistant [[hypertension]] and a decrease in estimated [[glomerular filtration rate]] (eGFR) in a patient known to have [[atherosclerosis]] are 3 elements that are very important to raise the suspicion of [[Atherosclerosis|atherosclerotic]] [[renal artery stenosis]]. Other factors, such as [[hypertension]] at an early age or [[malignant hypertension]], play a major role as well.

==History and symptoms==
According to the KDOQI Clinical Practice Guidelines on Hypertension and [[Antihypertensive]] Agents in [[Chronic kidney diseas|Chronic Kidney Disease]]<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>, the most important clinical clues that should raise the suspicion of renal artery disease are the triad:

* Resistant Hypertension
* Reduced in estimated [[Glomerular filtration rate|glomerular filteration rate]] (eGFR)
* Known generalized [[atherosclerosis]]

Additional clinical clues that suggest renal artery disease are listed below<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>:

*Age of [[hypertension]] < 30 years and > 55 years
*Abrupt onset of [[hypertension]]
*Accelerated [[hypertension]] that was previously well-controlled
*Refractory [[hypertension]] to 3 anti-hypertensive medications
*[[Malignant hypertension]]
*[[Smoking]]
*Abdominal bruit
*[[Flash pulmonary edema]]
*Generalized atherosclerosis obliterans
*Asymmetric [[kidney]] sizes
*[[Acute kidney injury]] when ACE-I or ARB are used for treatment

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis surgery

2020-12-15T23:42:17Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
While [[balloon angioplasty]] and [[surgery]] are associated with equal rates of improving renal function and [[hypertension]] in patients with [[renal artery stenosis]] (RAS), the higher rate of post-operative complications associated with the [[vascular]] surgical reconstruction makes [[angioplasty]] the preferred first-line treatment of [[RAS]] among [[patients]] requiring intervention. Vascular surgical reconstruction is reserved for a minority of cases. The need for surgical reoperation is 5-15%.

==Surgery==
[[Vascular]] [[surgical]] [[reconstruction]] is reserved for a minority of cases. Similar to all surgeries, vascular [[surgical]] reconstruction is associated with complications. The need for reoperation is documented in 5-15% of all [[Renal artery stenosis]] patients who require [[surgical]] [[intervention]].<ref name="pmid3051450">{{cite journal| author=Novick AC| title=Surgical correction of renovascular hypertension. | journal=Surg Clin North Am | year= 1988 | volume= 68 | issue= 5 | pages= 1007-25 | pmid=3051450 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3051450 }} </ref><ref name="pmid8028093">{{cite journal| author=Cambria RP, Brewster DC, L'Italien GJ, Moncure A, Darling RC, Gertler JP et al.| title=The durability of different reconstructive techniques for [[atherosclerotic]] [[renal artery disease]]. | journal=J Vasc Surg | year= 1994 | volume= 20 | issue= 1 | pages= 76-85; discussion 86-7 | pmid=8028093 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8028093 }} </ref><ref name="pmid3795433">{{cite journal| author=Novick AC, Ziegelbaum M, Vidt DG, Gifford RW, Pohl MA, Goormastic M| title=Trends in surgical revascularization for renal artery disease. Ten years' experience. | journal=JAMA | year= 1987 | volume= 257 | issue= 4 | pages= 498-501 | pmid=3795433 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3795433 }} </ref><ref name="pmid1593670">{{cite journal| author=Libertino JA, Bosco PJ, Ying CY, Breslin DJ, Woods BO, Tsapatsaris NP et al.| title=Renal revascularization to preserve and restore renal function. | journal=J Urol | year= 1992 | volume= 147 | issue= 6 | pages= 1485-7 | pmid=1593670 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1593670 }} </ref><ref name="pmid7776472">{{cite journal| author=Clair DG, Belkin M, Whittemore AD, Mannick JA, Donaldson MC| title=Safety and efficacy of transaortic renal endarterectomy as an adjunct to aortic surgery. | journal=J Vasc Surg | year= 1995 | volume= 21 | issue= 6 | pages= 926-33; discussion 934 | pmid=7776472 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7776472 }} </ref>

===Indications===
[[Vascular]] [[surgical]] [[reconstruction]] is indicated in specific cases of [[atherosclerotic]] [[RAS]]<ref name="pmid3051450">{{cite journal| author=Novick AC| title=Surgical correction of renovascular hypertension. | journal=Surg Clin North Am | year= 1988 | volume= 68 | issue= 5 | pages= 1007-25 | pmid=3051450 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3051450 }} </ref><ref name="pmid8028093">{{cite journal| author=Cambria RP, Brewster DC, L'Italien GJ, Moncure A, Darling RC, Gertler JP et al.| title=The durability of different reconstructive techniques for atherosclerotic renal artery disease. | journal=J Vasc Surg | year= 1994 | volume= 20 | issue= 1 | pages= 76-85; discussion 86-7 | pmid=8028093 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8028093 }} </ref><ref name="pmid3795433">{{cite journal| author=Novick AC, Ziegelbaum M, Vidt DG, Gifford RW, Pohl MA, Goormastic M| title=Trends in surgical revascularization for renal artery disease. Ten years' experience. | journal=JAMA | year= 1987 | volume= 257 | issue= 4 | pages= 498-501 | pmid=3795433 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3795433 }} </ref><ref name="pmid1593670">{{cite journal| author=Libertino JA, Bosco PJ, Ying CY, Breslin DJ, Woods BO, Tsapatsaris NP et al.| title=Renal revascularization to preserve and restore renal function. | journal=J Urol | year= 1992 | volume= 147 | issue= 6 | pages= 1485-7 | pmid=1593670 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1593670 }} </ref><ref name="pmid7776472">{{cite journal| author=Clair DG, Belkin M, Whittemore AD, Mannick JA, Donaldson MC| title=Safety and efficacy of transaortic renal endarterectomy as an adjunct to aortic surgery. | journal=J Vasc Surg | year= 1995 | volume= 21 | issue= 6 | pages= 926-33; discussion 934 | pmid=7776472 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7776472 }} </ref>:

*Involvement of multiple [[small arteries]]
*Involvement of early primary branching of the main [[renal artery]]
*[[Renal artery]] reconstruction during [[pararenal]] [[aortic reconstruction]] in cases such as [[aortic aneurysms]] or aortoiliac occlusive disease

===Risk Factors===
The risk of complications associated with [[renal artery]] [[reconstruction]] [[increases]] in the following conditions:<ref name="pmid3051450">{{cite journal| author=Novick AC| title=Surgical correction of renovascular hypertension. | journal=Surg Clin North Am | year= 1988 | volume= 68 | issue= 5 | pages= 1007-25 | pmid=3051450 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3051450 }} </ref><ref name="pmid8028093">{{cite journal| author=Cambria RP, Brewster DC, L'Italien GJ, Moncure A, Darling RC, Gertler JP et al.| title=The durability of different reconstructive techniques for atherosclerotic renal artery disease. | journal=J Vasc Surg | year= 1994 | volume= 20 | issue= 1 | pages= 76-85; discussion 86-7 | pmid=8028093 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8028093 }} </ref><ref name="pmid3795433">{{cite journal| author=Novick AC, Ziegelbaum M, Vidt DG, Gifford RW, Pohl MA, Goormastic M| title=Trends in surgical revascularization for renal artery disease. Ten years' experience. | journal=JAMA | year= 1987 | volume= 257 | issue= 4 | pages= 498-501 | pmid=3795433 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3795433 }} </ref><ref name="pmid1593670">{{cite journal| author=Libertino JA, Bosco PJ, Ying CY, Breslin DJ, Woods BO, Tsapatsaris NP et al.| title=Renal revascularization to preserve and restore renal function. | journal=J Urol | year= 1992 | volume= 147 | issue= 6 | pages= 1485-7 | pmid=1593670 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1593670 }} </ref><ref name="pmid7776472">{{cite journal| author=Clair DG, Belkin M, Whittemore AD, Mannick JA, Donaldson MC| title=Safety and efficacy of transaortic renal endarterectomy as an adjunct to aortic surgery. | journal=J Vasc Surg | year= 1995 | volume= 21 | issue= 6 | pages= 926-33; discussion 934 | pmid=7776472 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7776472 }} </ref>:

*Concomitant aortic reconstruction
*[[Renal insufficiency]]
*Use of aortic grafts as bypass graft

==Management of Patients With [[Peripheral]] [[Artery]] [[Disease]] (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines<ref name="pmid23473760">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2013 | volume= 61 | issue= 14 | pages= 1555-70 | pmid=23473760 | doi=10.1016/j.jacc.2013.01.004 | pmc=4492473 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23473760 }} </ref>==
{| class="wikitable"
|+
!Class I
!<nowiki>"</nowiki>'''1.''' Vascular surgical reconstruction is indicated for patients with [[Fibromuscular dysplasia|fibromuscular dysplastic RAS]] with clinical indications for interventions (same as for PTA), especially those exhibiting complex disease that extends into the segmental arteries and those having macroaneurysms. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''2.''' Vascular surgical reconstruction is indicated for patients with atherosclerotic RAS and clinical indications for intervention, especially those with multiple small [[renal arteries]] or early primary branching of the main renal artery. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''3.''' Vascular surgical reconstruction is indicated for patients with atherosclerotic RAS in combination with pararenal aortic reconstructions (in treatment of aortic aneurysms or severe [[aortoiliac occlusive disease]]). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>

|}
 
==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

{{WH}}
{{WS}}

Renal artery stenosis history and symptoms

2020-12-15T23:33:04Z

Shivam Singla: /* History and symptoms */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==
Resistant [[hypertension]] and a decrease in estimated [[glomerular filtration rate]] (eGFR) in a patient known to have [[atherosclerosis]] are 3 elements that are very important to raise the suspicion of [[Atherosclerosis|atherosclerotic]] [[renal artery stenosis]]. Other factors, such as [[hypertension]] at an early age or [[malignant hypertension]], play a major role as well.

==History and symptoms==
According to the KDOQI Clinical Practice Guidelines on Hypertension and [[Antihypertensive]] Agents in [[Chronic kidney diseas|Chronic Kidney Disease]]<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>, the most important clinical clues that should raise the suspicion of renal artery disease are the triad:

* Resistant Hypertension
* Reduced in estimated [[Glomerular filtration rate|glomerular filteration rate]] (eGFR)
* Known generalized [[atherosclerosis]]

Additional clinical clues that suggest renal artery disease are listed below<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>:

*Age of [[hypertension]] < 30 years and > 55 years
*Abrupt onset of [[hypertension]]
*Accelerated [[hypertension]] that was previously well-controlled
*Refractory [[hypertension]] to 3 anti-hypertensive medications
*[[Malignant hypertension]]
*[[Smoking]]
*Abdominal bruit
*[[Flash pulmonary edema]]
*Generalized atherosclerosis obliterans
*Asymmetric [[kidney]] sizes
*[[Acute kidney injury]] when ACE-I or ARB are used for treatment

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis epidemiology and demographics

2020-12-15T23:25:34Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}}; {{AE}} {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==

[[Renal artery stenosis|Atherosclerotic renal artery stenosis]] (ARAS) is considered a disease of the elderly. The true prevalence of [[ARAS]] has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Epidemiology and demographics==

[[Renal artery stenosis]] considered a disease of the elderly.<ref name="pmid11172181">{{cite journal| author=Safian RD, Textor SC| title=Renal-artery stenosis. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 6 | pages= 431-42 | pmid=11172181 | doi=10.1056/NEJM200102083440607 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11172181 }} </ref> It most commonly affects patients with cardiovascular co-morbidities, such as those with [[diabetes mellitus]], coronary and [[peripheral artery disease]], [[dyslipidemia]], [[essential hypertension]], and [[smoking]] history.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 |pages= 489-92 | pmid=2045754 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal functon changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>

*It is difficult to assess the real incidence and prevalence of renal artery stenosis because most patients with the disease are in fact asymptomatic.
*In one study that involved 14,152 patients undergoing [[Ultrasonography|abdominal aortography]], approximately 10% of the patients had [[Renal artery stenosis|RAS]] and 1.3% had bilateral [[Renal artery stenosis|RAS]], 60% of which were considered significant stenosis.<ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>
*Autopsy findings among 5194 patients between 1980 and 1988 showed that 4.3% of all patients [[Renal artery stenosis|RAS]], most of which were not diagnosed.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref> The frequency of [[Renal artery stenosis|RAS]] among patients with [[diabetes]] and [[hypertension]] was higher, reaching up to 10% of all patients. <ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
*Atherosclerotic [[renal artery stenosis]] affects approximately 0.5-7% of the U.S. population above the age of 65 years. It is present in almost 5% of patients with [[chronic kidney disease]].<ref name="pmid15954920">{{cite journal| author=Kalra PA, Guo H, Kausz AT, Gilbertson DT, Liu J, Chen SC et al.| title=Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 293-301 | pmid=15954920 | doi=10.1111/j.1523-1755.2005.00406.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954920 }} </ref><ref name="pmid12218965">{{cite journal| author=Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG et al.| title=Prevalence of renovascular disease in the elderly: a population-based study. | journal=J Vasc Surg | year= 2002 | volume= 36 | issue= 3 | pages= 443-51 | pmid=12218965 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12218965 }} </ref>
*Although stenosis may progress in 30-53% of patients within only 2-5 years. after diagnosis, only 3-15% of patient with [[Acute renal artery stenosis|ARAS]] progress to total occlusion of the [[renal arteries]].<ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal function changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg |year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9507221">{{cite journal| author=Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K et al.| title=Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. | journal=Kidney Int | year= 1998 | volume= 53 | issue= 3 | pages= 735-42 | pmid=9507221 | doi=10.1046/j.1523-1755.1998.00805.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9507221 }} </ref><ref name="pmid9860789">{{cite journal| author=Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ et al.| title=Prospective study of atherosclerotic disease progression in the renal artery. | journal=Circulation | year= 1998 | volume= 98 | issue= 25 | pages= 2866-72 | pmid=9860789 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9860789 }} </ref> The definition of disease progression, however, may vary between individual studies.
*To date, there is no reliable information about the prevalence of [[secondary hypertension]] due to [[renal artery stenosis]]. Follow-up and prognosis for hypertensive patients with [[renal artery stenosis]] has not yet been achieved.

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]
[[Category: Needs content]]

Renal artery stenosis classification

2020-12-15T23:21:43Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==

[[Renal artery stenosis]] classification is doner with the help of a doppler scanning of the [[renal artery]].

==Classification==

According to the American heart associated AHA classification, the [[renal artery stenosis]] is divided into grade I, II, III depending upon the [[Hypertension]]/[[Normotension]] and [[Renal function]].
According to AHA<ref name="urlRenal Artery Stenosis Guidelines: Guidelines Summary">{{cite web |url=https://emedicine.medscape.com/article/245023-guidelines |title=Renal Artery Stenosis Guidelines: Guidelines Summary |format= |work= |accessdate=}}</ref>

Grade 1- [[Renal artery stenosis]] is present but the [[patient]] is Normotensive with a normal [[renal function]].

Grade 2- [[Renal artery stenosis]] is present but the patient is having [[hypertension]] that is medically controlled with a normal [[renal]] function.

Grade 3- [[Renal artery stenosis]] is present but the patient is having [[hypertension]] or volume overloaded with abnormal [[renal]] function.

[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]]. Additionally, [[renal artery stenosis]] is often classified anatomically according to severity of luminal narrowing. The following criteria are used according to most published studies about [[atherosclerosis]] [[renal artery stenosis]].<ref name="pmid8234704">{{cite journal| author=Kliewer MA, Tupler RH, Carroll BA, Paine SS, Kriegshauser JS, Hertzberg BS et al.| title=Renal artery stenosis: analysis of Doppler waveform parameters and tardus-parvus pattern. | journal=Radiology | year= 1993 | volume= 189 | issue= 3 | pages= 779-87 |pmid=8234704 | doi=10.1148/radiology.189.3.8234704 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8234704 }} </ref><ref name="pmid2243982">{{cite journal| author=Desberg AL, Paushter DM, Lammert GK, Hale JC, Troy RB, Novick AC et al.| title=Renal artery stenosis: evaluation with color Doppler flow imaging. | journal=Radiology |year= 1990 | volume= 177 | issue= 3 | pages= 749-53 | pmid=2243982 | doi=10.1148/radiology.177.3.2243982 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2243982 }} </ref>
{|border="1" style="border-collapse:collapse; text-align:left; font-size:120%;" cellpadding="5" align="center" width="300px"
| bgcolor="#ff9a69" align="center"|'''Severity'''||bgcolor="#ff9a69" align="center"|'''Luminal Narrowing'''
|-
| bgcolor="#f3f3f3"| Normal
| 0%
|-
|bgcolor="#f3f3f3"| Mild
| 1-49%
|-
| bgcolor="#f3f3f3"| Moderate
| 50-69%
|-
| bgcolor="#f3f3f3"| Severe
| 70-99%
|-
| bgcolor="#f3f3f3"| Occluded
| 100%
|}

To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of [[atherosclerotic]] [[renal artery stenosis]] as narrowing > 50%.<ref name="pmid21719621">{{cite journal| author=Lao D, Parasher PS, Cho KC, Yeghiazarians Y| title=Atherosclerotic renal artery stenosis--diagnosis and treatment. | journal=Mayo Clin Proc | year= 2011 | volume= 86 | issue= 7 | pages= 649-57 |pmid=21719621 | doi=10.4065/mcp.2011.0181 | pmc=PMC3127560 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21719621 }} </ref>

Another classification is based on hemodynamic function in [[renal artery stenosis]]. This classification simply differentiates between hemodynamically insignificant [[renal artery stenosis]] (< 75% stenosis) and hemodynamically significant renal artery stenosis (> 75% stenosis).<ref name="pmid15114537">{{cite journal| author=Kidney Disease Outcomes Quality Initiative (K/DOQI)| title=K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. | journal=Am J Kidney Dis | year= 2004 | volume= 43 | issue= 5 Suppl 1 | pages= S1-290 | pmid=15114537 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15114537 }} </ref>

==References==

{{reflist|2}}

[[Category:Cardiology]]
[[Category:Kidney diseases]]
[[Category:Nephrology]]

Renal artery stenosis overview

2020-12-15T22:44:19Z

Shivam Singla: /* Overview */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the [[renal arteries]] or their proximal branches of more than 50% in diameter.
*[[Renal artery stenosis|RAS]] is a heterogeneous group of diseases that most commonly include: [[Fibromuscular dysplasia|fibromuscular dysplasia (FMD)]] and atherosclerotic renal artery stenosis (ARAS).
*Although [[renal artery stenosis]] may be an isolated asymptomatic condition,
*It may commonly lead to [[secondary hypertension]] that is thus called [[renovascular hypertension (RVHT)]], [[ischemic nephropathy]], and [[Chronic renal insufficiency|chronic renal insufficiency.]]

*Approximately 90% of [[renal artery stenosis]] cases occur due to progressive [[atherosclerosis]].
*The ostium and proximal third of the renal arteries are the most commonly involved regions in [[atherosclerosis]].
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of [[chronic kidney disease]] and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind [[renal artery stenosis]] is reduction in renal blood flow
*Secondary to [[renal artery stenosis]] which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor reflex]], and the [[sympathetic nervous system]].

*Elevated angiotensin II activities in turn cause elevation of the [[arterial pressure]] and other effects including [[Aldosterone|aldosterone secretion]], sodium retention, and [[left ventricular hypertrophy]] and remodeling.

==Causes==

*[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic plaque]] in the renal arteries (termed [[atherosclerotic]] renal artery stenosis).
*Less frequently, it is caused by [[fibromuscular dysplasia]].

==Classification==

*[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]].

*Additionally, [[renal artery stenosis]] is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in [[Renal artery stenosis|RAS]]. This classification simply differentiates between hemodynamically insignificant [[Renal artery stenosis]] (< 75% stenosis) and hemodynamically significant [[Renal artery stenosis]] (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic [[renal artery stenosis]] (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with [[cardiovascular]] co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**[[Atherosclerosis]]
**Advanced age
**[[Dyslipidemia]]
**[[Diabetes mellitus]]
**[[Smoking]]
**[[Hypertension]]

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of [[Renal artery stenosis|ARAS]].

*[[Doppler ultrasonography]], [[CTA]], and [[MRA]] may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as [[renal angiography]], is considered the gold standard for diagnosis and may be used when
*Concomitant [[Catheterization|catheterizations]] are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with [[ARAS]].

*Several [[anti-hypertensive]] [[medications]] have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of [[PAD]], [[ACE-I]] and [[CCB]] may be used in [[patients]] with RAS because they have an effect on both lowering BP and delaying the [[renal disease]].

*Other [[blood pressure]]-lowering medications include [[beta-blockers]], [[hydrazine]], and [[chlorothiazide]].

*Although [[ARBs]] may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*[[Angioplasty]] and [[stent]] implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the [[CORAL]] trial showed that although there are high technical success rates with [[angioplasty]]/[[stenting]], the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI ([[percutaneous renal interventions]]) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the [[renal arteries]] may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==Case studies==

==References==

Renal artery stenosis overview

2020-12-15T20:06:31Z

Shivam Singla: /* Treatment */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the [[renal arteries]] or their proximal branches of more than 50% in diameter.
*[[Renal artery stenosis|RAS]] is a heterogeneous group of diseases that most commonly include: [[Fibromuscular dysplasia|fibromuscular dysplasia (FMD)]] and atherosclerotic renal artery stenosis (ARAS).
*Although [[renal artery stenosis]] may be an isolated asymptomatic condition,
**It may commonly lead to [[secondary hypertension]] that is thus called [[renovascular hypertension (RVHT)]], [[ischemic nephropathy]], and [[Chronic renal insufficiency|chronic renal insufficiency.]]

*Approximately 90% of [[renal artery stenosis]] cases occur due to progressive [[atherosclerosis]].
*The ostium and proximal third of the renal arteries are the most commonly involved regions in [[atherosclerosis]].
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of [[chronic kidney disease]] and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind [[renal artery stenosis]] is reduction in renal blood flow
*Secondary to [[renal artery stenosis]] which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor reflex]], and the [[sympathetic nervous system]].

*Elevated angiotensin II activities in turn cause elevation of the [[arterial pressure]] and other effects including [[Aldosterone|aldosterone secretion]], sodium retention, and [[left ventricular hypertrophy]] and remodeling.

==Causes==

*[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic plaque]] in the renal arteries (termed [[atherosclerotic]] renal artery stenosis).
*Less frequently, it is caused by [[fibromuscular dysplasia]].

==Classification==

*[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]].

*Additionally, [[renal artery stenosis]] is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in [[Renal artery stenosis|RAS]]. This classification simply differentiates between hemodynamically insignificant [[Renal artery stenosis]] (< 75% stenosis) and hemodynamically significant [[Renal artery stenosis]] (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic [[renal artery stenosis]] (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with [[cardiovascular]] co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**[[Atherosclerosis]]
**Advanced age
**[[Dyslipidemia]]
**[[Diabetes mellitus]]
**[[Smoking]]
**[[Hypertension]]

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of [[Renal artery stenosis|ARAS]].

*[[Doppler ultrasonography]], [[CTA]], and [[MRA]] may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as [[renal angiography]], is considered the gold standard for diagnosis and may be used when
*Concomitant [[Catheterization|catheterizations]] are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with [[ARAS]].

*Several [[anti-hypertensive]] [[medications]] have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of [[PAD]], [[ACE-I]] and [[CCB]] may be used in [[patients]] with RAS because they have an effect on both lowering BP and delaying the [[renal disease]].

*Other [[blood pressure]]-lowering medications include [[beta-blockers]], [[hydrazine]], and [[chlorothiazide]].

*Although [[ARBs]] may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*[[Angioplasty]] and [[stent]] implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the [[CORAL]] trial showed that although there are high technical success rates with [[angioplasty]]/[[stenting]], the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI ([[percutaneous renal interventions]]) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the [[renal arteries]] may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==Case studies==

==References==

Renal artery stenosis overview

2020-12-15T19:28:34Z

Shivam Singla: /* Classification */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the [[renal arteries]] or their proximal branches of more than 50% in diameter.
*[[Renal artery stenosis|RAS]] is a heterogeneous group of diseases that most commonly include: [[Fibromuscular dysplasia|fibromuscular dysplasia (FMD)]] and atherosclerotic renal artery stenosis (ARAS).
*Although [[renal artery stenosis]] may be an isolated asymptomatic condition,
**It may commonly lead to [[secondary hypertension]] that is thus called [[renovascular hypertension (RVHT)]], [[ischemic nephropathy]], and [[Chronic renal insufficiency|chronic renal insufficiency.]]

*Approximately 90% of [[renal artery stenosis]] cases occur due to progressive [[atherosclerosis]].
*The ostium and proximal third of the renal arteries are the most commonly involved regions in [[atherosclerosis]].
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of [[chronic kidney disease]] and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind [[renal artery stenosis]] is reduction in renal blood flow
*Secondary to [[renal artery stenosis]] which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor reflex]], and the [[sympathetic nervous system]].

*Elevated angiotensin II activities in turn cause elevation of the [[arterial pressure]] and other effects including [[Aldosterone|aldosterone secretion]], sodium retention, and [[left ventricular hypertrophy]] and remodeling.

==Causes==

*[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic plaque]] in the renal arteries (termed [[atherosclerotic]] renal artery stenosis).
*Less frequently, it is caused by [[fibromuscular dysplasia]].

==Classification==

*[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]].

*Additionally, [[renal artery stenosis]] is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in [[Renal artery stenosis|RAS]]. This classification simply differentiates between hemodynamically insignificant [[Renal artery stenosis]] (< 75% stenosis) and hemodynamically significant [[Renal artery stenosis]] (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic [[renal artery stenosis]] (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with [[cardiovascular]] co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**[[Atherosclerosis]]
**Advanced age
**[[Dyslipidemia]]
**[[Diabetes mellitus]]
**[[Smoking]]
**[[Hypertension]]

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of [[Renal artery stenosis|ARAS]].

*[[Doppler ultrasonography]], [[CTA]], and [[MRA]] may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as [[renal angiography]], is considered the gold standard for diagnosis and may be used when
*Concomitant [[Catheterization|catheterizations]] are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with ARAS.

*Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

*Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

*Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==Case studies==

==References==

Renal artery stenosis overview

2020-12-15T19:27:04Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the [[renal arteries]] or their proximal branches of more than 50% in diameter.
*[[Renal artery stenosis|RAS]] is a heterogeneous group of diseases that most commonly include: [[Fibromuscular dysplasia|fibromuscular dysplasia (FMD)]] and atherosclerotic renal artery stenosis (ARAS).
*Although [[renal artery stenosis]] may be an isolated asymptomatic condition,
**It may commonly lead to [[secondary hypertension]] that is thus called [[renovascular hypertension (RVHT)]], [[ischemic nephropathy]], and [[Chronic renal insufficiency|chronic renal insufficiency.]]

*Approximately 90% of [[renal artery stenosis]] cases occur due to progressive [[atherosclerosis]].
*The ostium and proximal third of the renal arteries are the most commonly involved regions in [[atherosclerosis]].
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of [[chronic kidney disease]] and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind [[renal artery stenosis]] is reduction in renal blood flow
*Secondary to [[renal artery stenosis]] which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor reflex]], and the [[sympathetic nervous system]].

*Elevated angiotensin II activities in turn cause elevation of the [[arterial pressure]] and other effects including [[Aldosterone|aldosterone secretion]], sodium retention, and [[left ventricular hypertrophy]] and remodeling.

==Causes==

*[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic plaque]] in the renal arteries (termed [[atherosclerotic]] renal artery stenosis).
*Less frequently, it is caused by [[fibromuscular dysplasia]].

==Classification==

*[[Renal artery stenosis]] may be classified according to whether there is unilateral or bilateral involvement of the [[renal arteries]].

*Additionally, [[renal artery stenosis]] is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in [[Renal artery stenosis|RAS]]. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic [[renal artery stenosis]] (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with [[cardiovascular]] co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**[[Atherosclerosis]]
**Advanced age
**[[Dyslipidemia]]
**[[Diabetes mellitus]]
**[[Smoking]]
**[[Hypertension]]

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of [[Renal artery stenosis|ARAS]].

*[[Doppler ultrasonography]], [[CTA]], and [[MRA]] may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as [[renal angiography]], is considered the gold standard for diagnosis and may be used when
*Concomitant [[Catheterization|catheterizations]] are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with ARAS.

*Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

*Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

*Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==Case studies==

==References==

Renal artery stenosis overview

2020-12-15T19:19:28Z

Shivam Singla: /* Case Studies */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

*[[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.
*RAS is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS).
*Although renal artery stenosis may be an isolated asymptomatic condition,
**It may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

*Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis.
*The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.
*Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==

*The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow
*Secondary to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system.

*Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==

*Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis).
*Less frequently, it is caused by fibromuscular dysplasia.

==Classification==

*Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries.

*Additionally, renal artery stenosis is classified anatomically according to the severity of luminal narrowing.

*The following criteria are used according to most published studies about ARAS.

*To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
*Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

*Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly.

*The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

*The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==

*Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
**Atherosclerosis,
**Advanced age
**Dyslipidemia
**Diabetes mellitus
**Smoking
**Hypertension.

==Diagnosis==

*Non-invasive diagnosis is the first line for the screening of ARAS.

*Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS.

*The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when
*Concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==

*Medical therapy is considered the first line of management for patients with ARAS.

*Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

*Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

*Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

== Case studies ==

==References==

Renal artery stenosis overview

2020-12-15T19:17:51Z

Shivam Singla: /* Treatment */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

* [[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.
* RAS is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS).
* Although renal artery stenosis may be an isolated asymptomatic condition,
** It may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

* Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis.
* The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.
* Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==

* The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow
* Secondary to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system.

* Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==

* Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis).
* Less frequently, it is caused by fibromuscular dysplasia.

==Classification==

* Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries.

* Additionally, renal artery stenosis is classified anatomically according to the severity of luminal narrowing.

* The following criteria are used according to most published studies about ARAS.

* To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
* Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

* Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly.

* The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

* The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==

* Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
** Atherosclerosis,
** Advanced age
** Dyslipidemia
** Diabetes mellitus
** Smoking
** Hypertension.

==Diagnosis==

* Non-invasive diagnosis is the first line for the screening of ARAS.

* Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS.

* The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when
* Concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==
*Medical therapy is considered the first line of management for patients with ARAS.

*Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

*According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

*Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

*Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

*Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

*Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Case Studies==

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==External Links==

==References==

Renal artery stenosis overview

2020-12-15T19:17:15Z

Shivam Singla: /* Diagnosis */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

* [[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.
* RAS is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS).
* Although renal artery stenosis may be an isolated asymptomatic condition,
** It may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

* Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis.
* The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.
* Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==

* The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow
* Secondary to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system.

* Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==

* Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis).
* Less frequently, it is caused by fibromuscular dysplasia.

==Classification==

* Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries.

* Additionally, renal artery stenosis is classified anatomically according to the severity of luminal narrowing.

* The following criteria are used according to most published studies about ARAS.

* To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
* Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

* Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly.

* The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

* The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==

* Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
** Atherosclerosis,
** Advanced age
** Dyslipidemia
** Diabetes mellitus
** Smoking
** Hypertension.

==Diagnosis==

* Non-invasive diagnosis is the first line for the screening of ARAS.

* Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS.

* The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when
* Concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==
Medical therapy is considered the first line of management for patients with ARAS.

Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Case Studies==

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==External Links==

==References==

Renal artery stenosis overview

2020-12-15T19:16:55Z

Shivam Singla: /* Pathophysiology */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

* [[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.
* RAS is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS).
* Although renal artery stenosis may be an isolated asymptomatic condition,
** It may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

* Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis.
* The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.
* Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==

* The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow
* Secondary to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system.

* Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==

* Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis).
* Less frequently, it is caused by fibromuscular dysplasia.

==Classification==

* Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries.

* Additionally, renal artery stenosis is classified anatomically according to the severity of luminal narrowing.

* The following criteria are used according to most published studies about ARAS.

* To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
* Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

* Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly.

* The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

* The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==

* Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
** Atherosclerosis,
** Advanced age
** Dyslipidemia
** Diabetes mellitus
** Smoking
** Hypertension.

==Diagnosis==

* Non-invasive diagnosis is the first line for the screening of ARAS.

* Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS.

* The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when
** Concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==
Medical therapy is considered the first line of management for patients with ARAS.

Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Case Studies==

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==External Links==

==References==

Renal artery stenosis overview

2020-12-15T18:04:39Z

Shivam Singla: /* Overview */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

* [[Renal artery stenosis|Renal artery stenosis (RAS)]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter.
* RAS is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS).
* Although renal artery stenosis may be an isolated asymptomatic condition,
** It may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

* Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis.
* The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis.
* Segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==

* The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow
** 20 to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system.

* Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==

* Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis).
* Less frequently, it is caused by fibromuscular dysplasia.

==Classification==

* Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries.

* Additionally, renal artery stenosis is classified anatomically according to the severity of luminal narrowing.

* The following criteria are used according to most published studies about ARAS.

* To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
* Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==

* Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly.

* The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies.

* The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==

* Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are:
** Atherosclerosis,
** Advanced age
** Dyslipidemia
** Diabetes mellitus
** Smoking
** Hypertension.

==Diagnosis==

* Non-invasive diagnosis is the first line for the screening of ARAS.

* Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS.

* The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when
** Concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==
Medical therapy is considered the first line of management for patients with ARAS.

Several anti-hypertensive medications have proven to be efficacious in ARAS patients.

According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease.

Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide.

Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Case Studies==

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==External Links==

==References==

Renal artery stenosis overview

2020-12-15T17:55:13Z

Shivam Singla: /* Classification */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==
[[Renal artery stenosis]] is defined as the unilateral or bilateral progressive narrowing of the renal arteries or their proximal branches of more than 50% in diameter. It is a heterogeneous group of diseases that most commonly include: fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS). Although renal artery stenosis may be an isolated asymptomatic condition, it may commonly lead to secondary hypertension that is thus called renovascular hypertension (RVHT), ischemic nephropathy, and chronic renal insufficiency.

Approximately 90% of renal artery stenosis cases occur due to progressive atherosclerosis. The ostium and proximal third of the renal arteries are the most commonly involved regions in atherosclerosis. Nonetheless, segmental and diffuse atherosclerosis may still be seen in the minority of patients, especially in context of chronic kidney disease and poor renal survival.

==Pathophysiology==
The main pathophysiological mechanism behind renal artery stenosis is reduction in renal blood flow secondary to renal artery stenosis which stimulates renin release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, baroreceptor reflex, and the sympathetic nervous system. Elevated angiotensin II activities in turn cause elevation of the arterial pressure and other effects including aldosterone secretion, sodium retention, and left ventricular hypertrophy and remodeling.

==Causes==
Renal artery stenosis is most commonly caused by the development of atherosclerotic plaque in the renal arteries (termed atherosclerotic renal artery stenosis). Less frequently, it is caused by fibromuscular dysplasia.

==Classification==
Renal artery stenosis may be classified according to whether there is unilateral or bilateral involvement of the renal arteries. Additionally, renal artery stenosis is often classified anatomically according to the severity of luminal narrowing. The following criteria are used according to most published studies about ARAS.
To note, some studies have different classification criteria than those listed above, with "mild disease" starting after 50% of luminal narrowing. Such classification remains coherent with the definition of ARAS as narrowing > 50%.
Another classification is based on hemodynamic function in RAS. This classification simply differentiates between hemodynamically insignificant RAS (< 75% stenosis) and hemodynamically significant RAS (> 75% stenosis).

==Epidemiology and Demographics==
Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly. The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to the varying selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as diabetes mellitus, dyslipidemia, essential hypertension, and known coronary or peripheral artery disease.

==Risk Factors==
Risk factors for ARAS, per se, are poorly studied. The most commonly associated risk factors are those similar to other types of atherosclerosis, such as advanced age, dyslipidemia, diabetes mellitus, smoking, and hypertension.

==Diagnosis==
Non-invasive diagnosis is the first line for the screening of ARAS. Doppler ultrasonography, CTA, and MRA may all be used to diagnose ARAS. The invasive diagnostic technique, such as renal angiography, is considered the gold standard for diagnosis and may be used when concomitant catheterizations are needed or when previously performed non-invasive techniques yielded equivocal results.

==Treatment==
Medical therapy is considered the first line of management for patients with ARAS. Several anti-hypertensive medications have proven to be efficacious in ARAS patients. According to the 2013 ACC/AHA Guidelines for the Management of PAD, ACE-I and CCB may be used in patients with RAS because they have an effect on both lowering BP and delaying the renal disease. Other blood pressure-lowering medications include beta-blockers, hydrazine, and chlorothiazide. Although ARBs may be used as well, they still have level B evidence for use in ARAS because trials have not been conducted on the use of ARBs in such patients.

Angioplasty and stent implantation were previously recommended by the 2013 ACC/AHA Guidelines. However, emerging data from the CORAL trial showed that although there are high technical success rates with angioplasty/stenting, the clinical endpoints are inconsistently and modestly modified. Therefore, raising the suspicion that PRI (percutaneous renal interventions) can incur substantial costs without a significant public health advantage

Vascular reconstruction of the renal arteries may be indicated in a small minority of patients. However, surgical reconstruction is associated with complications and carries a 5-15% for surgical re-intervention.

==Case Studies==

==Related Chapters==

*[[Renovascular hypertension]]
*[[Acute renal failure]]
*[[Atherosclerosis]]
*[[Chronic glomerulonephritis]]
*[[Hypersensitivity nephropathy]]
*[[Hypertension]]
*[[Malignant hypertension]]
*[[Nephrosclerosis]]
*[[Renovascular hypertension]]
*[[Uremia]]

==External Links==

==References==

File:Renal stenosis.jpeg

2020-12-15T17:53:49Z

Shivam Singla: Image showing the narrowing in the bilateral renal artery stenosis

== Summary ==
Image showing the narrowing in the bilateral renal artery stenosis

Renal artery stenosis diagnostic criteria

2020-12-13T23:04:18Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
There are numerous tests and procedures involved in the detection of [[renal artery stenosis]]. [[Renal artery stenosis]] is best diagnosed with [[MRA]](Magnetic resonance Imaging), [[Doppler ultrasound]], [[Computed tomography]], [[renal scintigraphy]], peripheral renin levels, and [[renal vein sampling]]. Though these all modalities are used for making the diagnosis but still [[renal vein sampling]], [[renal scintigraphy]] is not the first choice for making the diagnosis of [[renal artery stenosis]] because of their low [[sensitivity]] and [[specificity]] which is around 38-40.

==Diagnosis==

There are numerous tests and procedures involved in the detection of [[renal artery stenosis]]. [[Renal artery stenosis]] is best diagnosed with [[MRA]](Magnetic resonance Imaging), [[Doppler ultrasound]], [[Computed tomography]], [[renal scintigraphy]], peripheral [[renin levels]], and [[renal vein]] sampling. Though these all modalities are used for making the diagnosis but still [[renal vein]] sampling, [[renal scintigraphy]] are not the first choice for making the diagnosis of [[renal artery stenosis]] because of their low [[sensitivity]] and [[specificity]]<ref name="pmid11960229">{{cite journal |vauthors=Napoli V, Pinto S, Bargellini I, Vignali C, Cioni R, Petruzzi P, Salvetti A, Bartolozzi C |title=Duplex ultrasonographic study of the renal arteries before and after renal artery stenting |journal=Eur Radiol |volume=12 |issue=4 |pages=796–803 |date=April 2002 |pmid=11960229 |doi=10.1007/s003300101121 |url=}}</ref><ref name="pmid8610560">{{cite journal |vauthors=Grenier N, Trillaud H, Combe C, Degrèze P, Jeandot R, Gosse P, Douws C, Palussière J |title=Diagnosis of renovascular hypertension: feasibility of captopril-sensitized dynamic MR imaging and comparison with captopril scintigraphy |journal=AJR Am J Roentgenol |volume=166 |issue=4 |pages=835–43 |date=April 1996 |pmid=8610560 |doi=10.2214/ajr.166.4.8610560 |url=}}</ref> which is around 38-40.

The imaging modalities may be considered diagnostic if the following objectives are met:

(1) [[Anatomic]] and or [[Hemodynamic]] abnormality

(2) Anatomic consequences and complications associated with [[renal artery stenosis]] (Post stenotic dilatation of [[renal artery]] can be seen with the use of [[CTA]] and [[MRA]], shrinkage of [[renal parenchyma]], with [[kidneys]] being < 8 cm.

(3) [[Functional]] and [[cellular]] consequences of [[renal artery stenosis]]

(4) [[Renal]] impairment criteria related to [[renovascular disease]] should be me<ref name="pmid16356793">{{cite journal |vauthors=Grenier N, Hauger O, Cimpean A, Pérot V |title=Update of renal imaging |journal=Semin Nucl Med |volume=36 |issue=1 |pages=3–15 |date=January 2006 |pmid=16356793 |doi=10.1053/j.semnuclmed.2005.08.001 |url=}}</ref>.

==='''Ultrasonography'''===
[[Ultrasonography]] is readily available, secure, and inexpensive, and consequently is usually the first imaging study used to detect [[Renal artery stenosis]]. Usually, the results and accuracy are operator dependent and range in between 60-90%<ref name="pmid19917332">{{cite journal |vauthors=Zhang HL, Sos TA, Winchester PA, Gao J, Prince MR |title=Renal artery stenosis: imaging options, pitfalls, and concerns |journal=Prog Cardiovasc Dis |volume=52 |issue=3 |pages=209–19 |date=2009 |pmid=19917332 |doi=10.1016/j.pcad.2009.10.003 |url=}}</ref>.
This modality helps in the assessment of

*[[Renal functional reserve]]
*[[Renal resistive index]]

A [[renal artery]] EDV >90cm/s<ref name="pmid11172177">{{cite journal |vauthors=Radermacher J, Chavan A, Bleck J, Vitzthum A, Stoess B, Gebel MJ, Galanski M, Koch KM, Haller H |title=Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis |journal=N Engl J Med |volume=344 |issue=6 |pages=410–7 |date=February 2001 |pmid=11172177 |doi=10.1056/NEJM200102083440603 |url=}}</ref> and RRI< 75-80<ref name="pmid11704015">{{cite journal |vauthors=Mukherjee D, Bhatt DL, Robbins M, Roffi M, Cho L, Reginelli J, Bajzer C, Navarro F, Yadav JS |title=Renal artery end-diastolic velocity and renal artery resistance index as predictors of outcome after renal stenting |journal=Am J Cardiol |volume=88 |issue=9 |pages=1064–6 |date=November 2001 |pmid=11704015 |doi=10.1016/s0002-9149(01)01996-8 |url=}}</ref> represents no [[microvascular disease]]. The hemodynamic significant abnormality is concluded with the presence of spectral broadening and increased velocity on [[USG]].

[[Reno aortic velocity]] ratio > 3.5 corresponds with 60% [[stenosis]]<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref> and RAPSV (Renal artery peak systolic velocity) greater than 150cm/s corresponds to 50% stenosis whereas velocity greater than 180cm/s corresponds to 60% stenosis<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref><ref name="pmid7569132">{{cite journal |vauthors=Hélénon O, el Rody F, Correas JM, Melki P, Chauveau D, Chrétien Y, Moreau JF |title=Color Doppler US of renovascular disease in native kidneys |journal=Radiographics |volume=15 |issue=4 |pages=833–54; discussion 854–65 |date=July 1995 |pmid=7569132 |doi=10.1148/radiographics.15.4.7569132 |url=}}</ref>. According to recent studies, the [[sensitivity]] and [[specificity]] of [[ultrasound-guided]] detection of [[renal artery stenosis]] are usually 85% and 92% respectively. Severe [[stenosis]] is diagnosed on [[USG]] with slowed [[systolic accelerations]] along with the decreased [[resistive index]]<ref name="pmid1620853">{{cite journal |vauthors=Stavros AT, Parker SH, Yakes WF, Chantelois AE, Burke BJ, Meyers PR, Schenck JJ |title=Segmental stenosis of the renal artery: pattern recognition of tardus and parvus abnormalities with duplex sonography |journal=Radiology |volume=184 |issue=2 |pages=487–92 |date=August 1992 |pmid=1620853 |doi=10.1148/radiology.184.2.1620853 |url=}}</ref>.

[[Quantitative]] criteria for diagnosing distal [[stenosis]] includes early peak [[systolic]] acceleration <3m/s2, an acceleration index > 4m/s2, and or greater than 5% difference in [[RRI]] between both the [[kidneys]]. Because these waveforms are difficult to interpret these criteria are difficult to interpret<ref name="pmid12823921">{{cite journal |vauthors=Conkbayir I, Yücesoy C, Edgüer T, Yanik B, Yaşar Ayaz U, Hekimoğlu B |title=Doppler sonography in renal artery stenosis. An evaluation of intrarenal and extrarenal imaging parameters |journal=Clin Imaging |volume=27 |issue=4 |pages=256–60 |date=2003 |pmid=12823921 |doi=10.1016/s0899-7071(02)00547-8 |url=}}</ref><ref name="pmid8983584">{{cite journal |vauthors=Baxter GM, Aitchison F, Sheppard D, Moss JG, McLeod MJ, Harden PN, Love JG, Robertson M, Taylor G |title=Colour Doppler ultrasound in renal artery stenosis: intrarenal waveform analysis |journal=Br J Radiol |volume=69 |issue=825 |pages=810–5 |date=September 1996 |pmid=8983584 |doi=10.1259/0007-1285-69-825-810 |url=}}</ref>.

===Computed Tomographic Angiography.===
[[CT angiography]] provides a three-dimensional assessment of the tissue as one of the important tools in the diagnosis of [[Renal artery stenosis]].

*Contraindicated in patients with [[contrast allergy]] as this procedure modality involves the [[ionizing radiations]] and [[iodinated]] [[contrast]] medium.
*In [[patients]] having underlying [[renal impairment]] the use of [[iodinated contrast]] can lead to the development of [[contrast-induced nephropathy]], but it can be prevented with the use of [[hydration]] before doing the procedure.
*The [[sensitivity]] of this procedure is extremely high with 94% and [[specificity]] varies between 60% to 90 %<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>.
*[[CTA]] can give the detailed resolution of even small [[accessory renal arteries]].
*It is also the diagnostic modality of choice in patients having limited capacity to hold breath and also in patients having [[claustrophobia]].
*At the same time, [[CTA]] is having limited diagnostic modality as compared to [[MRA]] in detecting clinically significant [[Renal artery stenosis]] and also in patients having [[renal]] dysfunction 

===Magnetic Resonance Angiography===
[[MRA]] is having [[sensitivity]] and [[specificity]] of 90-100%<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>

*This procedure does not involve the use of [[iodinated contrast]] or [[radiations]], unlike [[CTA]].
*In patients with intermediate to [[end-stage renal failure]] due to the risk of [[nephrogenic]] systemic [[fibrosis]], [[gadolinium-based contrast media]] should be avoided.
*Additionally, In patients with the kind of implanted devices (i.e., [[pacemakers]], [[defibrillators]], [[cochlear implants]], and [[spinal cord stimulators]]), or in [[claustrophobic]] patients, [[MRA]] should not be used.
*[[Contrast]] reaction associated with [[MRA]] is lower as compared to [[CTA]]

===Angiography===
Invasive [[renal arteriography]] is an important helpful modality used these days in evaluating [[Renal artery stenosis]].

*[[Angiography]] can detect intrarenal [[vascular]] abnormalities and [[anatomical]] abnormalities of the [[kidneys]], [[renal arteries]], and [[aorta]], in addition to evaluating the severity of [[RAS]].
*[[Digital angiography]] by subtraction increases contrast resolution and can minimize the amount of [[contrast]] required to as little as 15mL.
*There are risks involved with [[arterial puncture]] and catheter/wire stimulation because [[renal angiography]] is invasive, which may lead to [[arterial damage]], [[spasm]], or [[thromboembolic phenomena]]<ref name="pmid7500898">{{cite journal |vauthors=Thadhani RI, Camargo CA, Xavier RJ, Fang LS, Bazari H |title=Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases |journal=Medicine (Baltimore) |volume=74 |issue=6 |pages=350–8 |date=November 1995 |pmid=7500898 |doi=10.1097/00005792-199511000-00005 |url=}}</ref>.
*[[Carbon dioxide]] should be used as a [[non-nephrotoxic]] [[contrast]] agent in patients with [[renal failure]] or [[contrast allergy]].
*To assess hemodynamic importance before conducting therapeutic procedures such as [[percutaneous transluminal renal angioplasty]] (PTRA) or stenting, translesional pressure gradients may be measured across regions of [[stenosis]].

==References==
<references />

Renal artery stenosis diagnostic criteria

2020-12-13T22:54:18Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
There are numerous tests and procedures involved in the detection of [[renal artery stenosis]]. [[Renal artery stenosis]] is best diagnosed with [[MRA]](Magnetic resonance Imaging), [[Doppler ultrasound]], [[Computed tomography]], [[renal scintigraphy]], peripheral renin levels, and [[renal vein sampling]]. Though these all modalities are used for making the diagnosis but still [[renal vein sampling]], [[renal scintigraphy]] is not the first choice for making the diagnosis of [[renal artery stenosis]] because of their low [[sensitivity]] and [[specificity]] which is around 38-40.

==Diagnosis==

There are numerous tests and procedures involved in the detection of [[renal artery stenosis]]. [[Renal artery stenosis]] is best diagnosed with [[MRA]](Magnetic resonance Imaging), [[Doppler ultrasound]], [[Computed tomography]], [[renal scintigraphy]], peripheral [[renin levels]], and [[renal vein]] sampling. Though these all modalities are used for making the diagnosis but still [[renal vein]] sampling, [[renal scintigraphy]] are not the first choice for making the diagnosis of [[renal artery stenosis]] because of their low [[sensitivity]] and [[specificity]]<ref name="pmid11960229">{{cite journal |vauthors=Napoli V, Pinto S, Bargellini I, Vignali C, Cioni R, Petruzzi P, Salvetti A, Bartolozzi C |title=Duplex ultrasonographic study of the renal arteries before and after renal artery stenting |journal=Eur Radiol |volume=12 |issue=4 |pages=796–803 |date=April 2002 |pmid=11960229 |doi=10.1007/s003300101121 |url=}}</ref><ref name="pmid8610560">{{cite journal |vauthors=Grenier N, Trillaud H, Combe C, Degrèze P, Jeandot R, Gosse P, Douws C, Palussière J |title=Diagnosis of renovascular hypertension: feasibility of captopril-sensitized dynamic MR imaging and comparison with captopril scintigraphy |journal=AJR Am J Roentgenol |volume=166 |issue=4 |pages=835–43 |date=April 1996 |pmid=8610560 |doi=10.2214/ajr.166.4.8610560 |url=}}</ref> which is around 38-40.

The imaging modalities may be considered diagnostic if the following objectives are met:

(1) [[Anatomic]] and or [[Hemodynamic]] abnormality

(2) Anatomic consequences and complications associated with [[renal artery stenosis]] (Post stenotic dilatation of [[renal artery]] can be seen with the use of [[CTA]] and [[MRA]], shrinkage of [[renal parenchyma]], with [[kidneys]] being < 8 cm.

(3) [[Functional]] and [[cellular]] consequences of [[renal artery stenosis]]

(4) [[Renal]] impairment criteria related to [[renovascular disease]] should be me<ref name="pmid16356793">{{cite journal |vauthors=Grenier N, Hauger O, Cimpean A, Pérot V |title=Update of renal imaging |journal=Semin Nucl Med |volume=36 |issue=1 |pages=3–15 |date=January 2006 |pmid=16356793 |doi=10.1053/j.semnuclmed.2005.08.001 |url=}}</ref>.

==='''Ultrasonography'''===
[[Ultrasonography]] is readily available, secure, and inexpensive, and consequently is usually the first imaging study used to detect [[Renal artery stenosis]]. Usually, the results and accuracy are operator dependent and range in between 60-90%<ref name="pmid19917332">{{cite journal |vauthors=Zhang HL, Sos TA, Winchester PA, Gao J, Prince MR |title=Renal artery stenosis: imaging options, pitfalls, and concerns |journal=Prog Cardiovasc Dis |volume=52 |issue=3 |pages=209–19 |date=2009 |pmid=19917332 |doi=10.1016/j.pcad.2009.10.003 |url=}}</ref>.
This modality helps in the assessment of

*[[Renal functional reserve]]
*[[Renal resistive index]]

A [[renal artery]] EDV >90cm/s<ref name="pmid11172177">{{cite journal |vauthors=Radermacher J, Chavan A, Bleck J, Vitzthum A, Stoess B, Gebel MJ, Galanski M, Koch KM, Haller H |title=Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis |journal=N Engl J Med |volume=344 |issue=6 |pages=410–7 |date=February 2001 |pmid=11172177 |doi=10.1056/NEJM200102083440603 |url=}}</ref> and RRI< 75-80<ref name="pmid11704015">{{cite journal |vauthors=Mukherjee D, Bhatt DL, Robbins M, Roffi M, Cho L, Reginelli J, Bajzer C, Navarro F, Yadav JS |title=Renal artery end-diastolic velocity and renal artery resistance index as predictors of outcome after renal stenting |journal=Am J Cardiol |volume=88 |issue=9 |pages=1064–6 |date=November 2001 |pmid=11704015 |doi=10.1016/s0002-9149(01)01996-8 |url=}}</ref> represents no [[microvascular disease]]. The hemodynamic significant abnormality is concluded with the presence of spectral broadening and increased velocity on [[USG]].

[[Reno aortic velocity]] ratio > 3.5 corresponds with 60% [[stenosis]]<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref> and RAPSV (Renal artery peak systolic velocity) greater than 150cm/s corresponds to 50% stenosis whereas velocity greater than 180cm/s corresponds to 60% stenosis<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref><ref name="pmid7569132">{{cite journal |vauthors=Hélénon O, el Rody F, Correas JM, Melki P, Chauveau D, Chrétien Y, Moreau JF |title=Color Doppler US of renovascular disease in native kidneys |journal=Radiographics |volume=15 |issue=4 |pages=833–54; discussion 854–65 |date=July 1995 |pmid=7569132 |doi=10.1148/radiographics.15.4.7569132 |url=}}</ref>. According to recent studies, the [[sensitivity]] and [[specificity]] of [[ultrasound-guided]] detection of [[renal artery stenosis]] are usually 85% and 92% respectively. Severe [[stenosis]] is diagnosed on [[USG]] with slowed [[systolic accelerations]] along with the decreased [[resistive index]]<ref name="pmid1620853">{{cite journal |vauthors=Stavros AT, Parker SH, Yakes WF, Chantelois AE, Burke BJ, Meyers PR, Schenck JJ |title=Segmental stenosis of the renal artery: pattern recognition of tardus and parvus abnormalities with duplex sonography |journal=Radiology |volume=184 |issue=2 |pages=487–92 |date=August 1992 |pmid=1620853 |doi=10.1148/radiology.184.2.1620853 |url=}}</ref>.

Quantitative criteria for diagnosing distal stenosis includes early peak systolic acceleration <3m/s2, an acceleration index > 4m/s2, and or greater than 5% difference in RRI between both the kidneys. Because these waveforms are difficult to interpret these criteria are difficult to interpret<ref name="pmid12823921">{{cite journal |vauthors=Conkbayir I, Yücesoy C, Edgüer T, Yanik B, Yaşar Ayaz U, Hekimoğlu B |title=Doppler sonography in renal artery stenosis. An evaluation of intrarenal and extrarenal imaging parameters |journal=Clin Imaging |volume=27 |issue=4 |pages=256–60 |date=2003 |pmid=12823921 |doi=10.1016/s0899-7071(02)00547-8 |url=}}</ref><ref name="pmid8983584">{{cite journal |vauthors=Baxter GM, Aitchison F, Sheppard D, Moss JG, McLeod MJ, Harden PN, Love JG, Robertson M, Taylor G |title=Colour Doppler ultrasound in renal artery stenosis: intrarenal waveform analysis |journal=Br J Radiol |volume=69 |issue=825 |pages=810–5 |date=September 1996 |pmid=8983584 |doi=10.1259/0007-1285-69-825-810 |url=}}</ref>.

===Computed Tomographic Angiography.===
CT angiography provides a three-dimensional assessment of the tissue as one of the important tools in the diagnosis of Renal artery stenosis.

*Contraindicated in patients with contrast allergy as this procedure modality involves the ionizing radiations and iodinated contrast medium.
*In patients having underlying renal impairment the use of iodinated contrast can lead to the development of contrast-induced nephropathy, but it can be prevented with the use of hydration before doing the procedure.
*The sensitivity of this procedure is extremely high with 94% and specificity varies between 60% to 90 %<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>.
*CTA can give the detailed resolution of even small accessory renal arteries.
*It is also the diagnostic modality of choice in patients having limited capacity to hold breath and also in patients having claustrophobia.
*At the same time, CTA is having limited diagnostic modality as compared to MRA in detecting clinically significant Renal artery stenosis and also in patients having renal dysfunction 

===Magnetic Resonance Angiography===
MRA is having sensitivity and specificity of 90-100%<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>

*This procedure does not involve the use of iodinated contrast or radiations, unlike CTA.
*In patients with intermediate to end-stage renal failure due to the risk of nephrogenic systemic fibrosis, gadolinium-based contrast media should be avoided.
*Additionally, In patients with the kind of implanted devices (i.e., pacemakers, defibrillators, cochlear implants, and spinal cord stimulators), or in claustrophobic patients, MRA should not be used.
*Contrast reaction associated with MRA is lower as compared to CTA

===Angiography===
Invasive renal arteriography is an important helpful modality used these days in evaluating Renal artery stenosis.

*Angiography can detect intrarenal vascular abnormalities and anatomical abnormalities of the kidneys, renal arteries, and aorta, in addition to evaluating the severity of RAS.
*Digital angiography by subtraction increases contrast resolution and can minimize the amount of contrast required to as little as 15mL.
*There are risks involved with arterial puncture and catheter/wire stimulation because renal angiography is invasive, which may lead to arterial damage, spasm, or thromboembolic phenomena<ref name="pmid7500898">{{cite journal |vauthors=Thadhani RI, Camargo CA, Xavier RJ, Fang LS, Bazari H |title=Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases |journal=Medicine (Baltimore) |volume=74 |issue=6 |pages=350–8 |date=November 1995 |pmid=7500898 |doi=10.1097/00005792-199511000-00005 |url=}}</ref>.
*Carbon dioxide should be used as a non-nephrotoxic contrast agent in patients with renal failure or contrast allergy.
*To assess hemodynamic importance before conducting therapeutic procedures such as percutaneous transluminal renal angioplasty (PTRA) or stenting, translesional pressure gradients may be measured across regions of stenosis.

==References==
<references />

Renal artery stenosis diagnostic criteria

2020-12-13T22:48:02Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
There are numerous tests and procedures involved in the detection of [[renal artery stenosis]]. [[Renal artery stenosis]] is best diagnosed with [[MRA]](Magnetic resonance Imaging), [[Doppler ultrasound]], [[Computed tomography]], [[renal scintigraphy]], peripheral renin levels, and [[renal vein sampling]]. Though these all modalities are used for making the diagnosis but still [[renal vein sampling]], [[renal scintigraphy]] is not the first choice for making the diagnosis of [[renal artery stenosis]] because of their low [[sensitivity]] and [[specificity]] which is around 38-40.

==Diagnosis==

There are numerous tests and procedures involved in the detection of renal artery stenosis. Renal artery stenosis is best diagnosed with MRA(Magnetic resonance Imaging), Doppler ultrasound, Computed tomography, renal scintigraphy, peripheral renin levels, and renal vein sampling. Though these all modalities are used for making the diagnosis but still renal vein sampling, renal scintigraphy are not the first choice for making the diagnosis of renal artery stenosis because of their low sensitivity and specificity<ref name="pmid11960229">{{cite journal |vauthors=Napoli V, Pinto S, Bargellini I, Vignali C, Cioni R, Petruzzi P, Salvetti A, Bartolozzi C |title=Duplex ultrasonographic study of the renal arteries before and after renal artery stenting |journal=Eur Radiol |volume=12 |issue=4 |pages=796–803 |date=April 2002 |pmid=11960229 |doi=10.1007/s003300101121 |url=}}</ref><ref name="pmid8610560">{{cite journal |vauthors=Grenier N, Trillaud H, Combe C, Degrèze P, Jeandot R, Gosse P, Douws C, Palussière J |title=Diagnosis of renovascular hypertension: feasibility of captopril-sensitized dynamic MR imaging and comparison with captopril scintigraphy |journal=AJR Am J Roentgenol |volume=166 |issue=4 |pages=835–43 |date=April 1996 |pmid=8610560 |doi=10.2214/ajr.166.4.8610560 |url=}}</ref> which is around 38-40.

The imaging modalities may be considered diagnostic if the following objectives are met:

(1) Anatomic and or Hemodynamic abnormality

(2) Anatomic consequences and complications associated with renal artery stenosis (Post stenotic dilatation of renal artery can be seen with the use of CTA and MRA, shrinkage of renal parenchyma, with kidneys being < 8 cm.

(3) Functional and cellular consequences of renal artery stenosis

(4) Renal impairment criteria related to renovascular disease should be me<ref name="pmid16356793">{{cite journal |vauthors=Grenier N, Hauger O, Cimpean A, Pérot V |title=Update of renal imaging |journal=Semin Nucl Med |volume=36 |issue=1 |pages=3–15 |date=January 2006 |pmid=16356793 |doi=10.1053/j.semnuclmed.2005.08.001 |url=}}</ref>.

==='''Ultrasonography'''===
Ultrasonography is readily available, secure, and inexpensive, and consequently is usually the first imaging study used to detect Renal artery stenosis. Usually, the results and accuracy are operator dependent and range in between 60-90%<ref name="pmid19917332">{{cite journal |vauthors=Zhang HL, Sos TA, Winchester PA, Gao J, Prince MR |title=Renal artery stenosis: imaging options, pitfalls, and concerns |journal=Prog Cardiovasc Dis |volume=52 |issue=3 |pages=209–19 |date=2009 |pmid=19917332 |doi=10.1016/j.pcad.2009.10.003 |url=}}</ref>.
This modality helps in the assessment of

*Renal functional reserve
*Renal resistive index.

A renal artery EDV >90cm/s<ref name="pmid11172177">{{cite journal |vauthors=Radermacher J, Chavan A, Bleck J, Vitzthum A, Stoess B, Gebel MJ, Galanski M, Koch KM, Haller H |title=Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis |journal=N Engl J Med |volume=344 |issue=6 |pages=410–7 |date=February 2001 |pmid=11172177 |doi=10.1056/NEJM200102083440603 |url=}}</ref> and RRI< 75-80<ref name="pmid11704015">{{cite journal |vauthors=Mukherjee D, Bhatt DL, Robbins M, Roffi M, Cho L, Reginelli J, Bajzer C, Navarro F, Yadav JS |title=Renal artery end-diastolic velocity and renal artery resistance index as predictors of outcome after renal stenting |journal=Am J Cardiol |volume=88 |issue=9 |pages=1064–6 |date=November 2001 |pmid=11704015 |doi=10.1016/s0002-9149(01)01996-8 |url=}}</ref> represents no microvascular disease. The hemodynamic significant abnormality is concluded with the presence of spectral broadening and increased velocity on USG.

Reno aortic velocity ratio > 3.5 corresponds with 60% stenosis<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref> and RAPSV (Renal artery peak systolic velocity) greater than 150cm/s corresponds to 50% stenosis whereas velocity greater than 180cm/s corresponds to 60% stenosis<ref name="pmid7741367">{{cite journal |vauthors=Olin JW, Piedmonte MR, Young JR, DeAnna S, Grubb M, Childs MB |title=The utility of duplex ultrasound scanning of the renal arteries for diagnosing significant renal artery stenosis |journal=Ann Intern Med |volume=122 |issue=11 |pages=833–8 |date=June 1995 |pmid=7741367 |doi=10.7326/0003-4819-122-11-199506010-00004 |url=}}</ref><ref name="pmid7569132">{{cite journal |vauthors=Hélénon O, el Rody F, Correas JM, Melki P, Chauveau D, Chrétien Y, Moreau JF |title=Color Doppler US of renovascular disease in native kidneys |journal=Radiographics |volume=15 |issue=4 |pages=833–54; discussion 854–65 |date=July 1995 |pmid=7569132 |doi=10.1148/radiographics.15.4.7569132 |url=}}</ref>. According to recent studies, the sensitivity and specificity of ultrasound-guided detection of renal artery stenosis are usually 85% and 92% respectively. Severe stenosis is diagnosed on USG with slowed systolic accelerations along with the decreased resistive index<ref name="pmid1620853">{{cite journal |vauthors=Stavros AT, Parker SH, Yakes WF, Chantelois AE, Burke BJ, Meyers PR, Schenck JJ |title=Segmental stenosis of the renal artery: pattern recognition of tardus and parvus abnormalities with duplex sonography |journal=Radiology |volume=184 |issue=2 |pages=487–92 |date=August 1992 |pmid=1620853 |doi=10.1148/radiology.184.2.1620853 |url=}}</ref>.

Quantitative criteria for diagnosing distal stenosis includes early peak systolic acceleration <3m/s2, an acceleration index > 4m/s2, and or greater than 5% difference in RRI between both the kidneys. Because these waveforms are difficult to interpret these criteria are difficult to interpret<ref name="pmid12823921">{{cite journal |vauthors=Conkbayir I, Yücesoy C, Edgüer T, Yanik B, Yaşar Ayaz U, Hekimoğlu B |title=Doppler sonography in renal artery stenosis. An evaluation of intrarenal and extrarenal imaging parameters |journal=Clin Imaging |volume=27 |issue=4 |pages=256–60 |date=2003 |pmid=12823921 |doi=10.1016/s0899-7071(02)00547-8 |url=}}</ref><ref name="pmid8983584">{{cite journal |vauthors=Baxter GM, Aitchison F, Sheppard D, Moss JG, McLeod MJ, Harden PN, Love JG, Robertson M, Taylor G |title=Colour Doppler ultrasound in renal artery stenosis: intrarenal waveform analysis |journal=Br J Radiol |volume=69 |issue=825 |pages=810–5 |date=September 1996 |pmid=8983584 |doi=10.1259/0007-1285-69-825-810 |url=}}</ref>.

===Computed Tomographic Angiography.===
CT angiography provides a three-dimensional assessment of the tissue as one of the important tools in the diagnosis of Renal artery stenosis.

*Contraindicated in patients with contrast allergy as this procedure modality involves the ionizing radiations and iodinated contrast medium.
*In patients having underlying renal impairment the use of iodinated contrast can lead to the development of contrast-induced nephropathy, but it can be prevented with the use of hydration before doing the procedure.
*The sensitivity of this procedure is extremely high with 94% and specificity varies between 60% to 90 %<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>.
*CTA can give the detailed resolution of even small accessory renal arteries.
*It is also the diagnostic modality of choice in patients having limited capacity to hold breath and also in patients having claustrophobia.
*At the same time, CTA is having limited diagnostic modality as compared to MRA in detecting clinically significant Renal artery stenosis and also in patients having renal dysfunction 

===Magnetic Resonance Angiography===
MRA is having sensitivity and specificity of 90-100%<ref name="pmid17050355">{{cite journal |vauthors=Eklöf H, Ahlström H, Magnusson A, Andersson LG, Andrén B, Hägg A, Bergqvist D, Nyman R |title=A prospective comparison of duplex ultrasonography, captopril renography, MRA, and CTA in assessing renal artery stenosis |journal=Acta Radiol |volume=47 |issue=8 |pages=764–74 |date=October 2006 |pmid=17050355 |doi=10.1080/02841850600849092 |url=}}</ref><ref name="pmid17497443">{{cite journal |vauthors=Rountas C, Vlychou M, Vassiou K, Liakopoulos V, Kapsalaki E, Koukoulis G, Fezoulidis IV, Stefanidis I |title=Imaging modalities for renal artery stenosis in suspected renovascular hypertension: prospective intraindividual comparison of color Doppler US, CT angiography, GD-enhanced MR angiography, and digital substraction angiography |journal=Ren Fail |volume=29 |issue=3 |pages=295–302 |date=2007 |pmid=17497443 |doi=10.1080/08860220601166305 |url=}}</ref>

*This procedure does not involve the use of iodinated contrast or radiations, unlike CTA.
*In patients with intermediate to end-stage renal failure due to the risk of nephrogenic systemic fibrosis, gadolinium-based contrast media should be avoided.
*Additionally, In patients with the kind of implanted devices (i.e., pacemakers, defibrillators, cochlear implants, and spinal cord stimulators), or in claustrophobic patients, MRA should not be used.
*Contrast reaction associated with MRA is lower as compared to CTA

===Angiography===
Invasive renal arteriography is an important helpful modality used these days in evaluating Renal artery stenosis.

*Angiography can detect intrarenal vascular abnormalities and anatomical abnormalities of the kidneys, renal arteries, and aorta, in addition to evaluating the severity of RAS.
*Digital angiography by subtraction increases contrast resolution and can minimize the amount of contrast required to as little as 15mL.
*There are risks involved with arterial puncture and catheter/wire stimulation because renal angiography is invasive, which may lead to arterial damage, spasm, or thromboembolic phenomena<ref name="pmid7500898">{{cite journal |vauthors=Thadhani RI, Camargo CA, Xavier RJ, Fang LS, Bazari H |title=Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases |journal=Medicine (Baltimore) |volume=74 |issue=6 |pages=350–8 |date=November 1995 |pmid=7500898 |doi=10.1097/00005792-199511000-00005 |url=}}</ref>.
*Carbon dioxide should be used as a non-nephrotoxic contrast agent in patients with renal failure or contrast allergy.
*To assess hemodynamic importance before conducting therapeutic procedures such as percutaneous transluminal renal angioplasty (PTRA) or stenting, translesional pressure gradients may be measured across regions of stenosis.

==References==
<references />

Renal artery stenosis epidemiology and demographics

2020-12-12T22:23:02Z

Shivam Singla: /* Epidemiology and demographics */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}}; {{AE}} {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==

[[Renal artery stenosis|Atherosclerotic renal artery stenosis]] (ARAS) is considered a disease of the elderly. The true prevalence of [[ARAS]] has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Epidemiology and demographics==

[[Renal artery stenosis]] considered a disease of the elderly.<ref name="pmid11172181">{{cite journal| author=Safian RD, Textor SC| title=Renal-artery stenosis. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 6 | pages= 431-42 | pmid=11172181 | doi=10.1056/NEJM200102083440607 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11172181 }} </ref> It most commonly affects patients with cardiovascular co-morbidities, such as those with [[diabetes mellitus]], coronary and [[peripheral artery disease]], [[dyslipidemia]], [[essential hypertension]], and [[smoking]] history.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 |pages= 489-92 | pmid=2045754 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal functon changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>

*It is difficult to assess the real incidence and prevalence of renal artery stenosis because most patients with the disease are in fact asymptomatic.
*In one study that involved 14,152 patients undergoing [[Ultrasonography|abdominal aortography]], approximately 10% of the patients had [[Renal artery stenosis|RAS]] and 1.3% had bilateral [[Renal artery stenosis|RAS]], 60% of which were considered significant stenosis.<ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>
*Autopsy findings among 5194 patients between 1980 and 1988 showed that 4.3% of all patients [[Renal artery stenosis|RAS]], most of which were not diagnosed.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref> The frequency of RAS among patients with [[diabetes]] and [[hypertension]] was higher, reaching up to 10% of all patients. <ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
*Atherosclerotic [[renal artery stenosis]] affects approximately 0.5-7% of the U.S. population above the age of 65 years. It is present in almost 5% of patients with [[chronic kidney disease]].<ref name="pmid15954920">{{cite journal| author=Kalra PA, Guo H, Kausz AT, Gilbertson DT, Liu J, Chen SC et al.| title=Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 293-301 | pmid=15954920 | doi=10.1111/j.1523-1755.2005.00406.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954920 }} </ref><ref name="pmid12218965">{{cite journal| author=Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG et al.| title=Prevalence of renovascular disease in the elderly: a population-based study. | journal=J Vasc Surg | year= 2002 | volume= 36 | issue= 3 | pages= 443-51 | pmid=12218965 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12218965 }} </ref>
*Although stenosis may progress in 30-53% of patients within only 2-5 years. after diagnosis, only 3-15% of patient with [[Acute renal artery stenosis|ARAS]] progress to total occlusion of the [[renal arteries]].<ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal function changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg |year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9507221">{{cite journal| author=Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K et al.| title=Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. | journal=Kidney Int | year= 1998 | volume= 53 | issue= 3 | pages= 735-42 | pmid=9507221 | doi=10.1046/j.1523-1755.1998.00805.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9507221 }} </ref><ref name="pmid9860789">{{cite journal| author=Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ et al.| title=Prospective study of atherosclerotic disease progression in the renal artery. | journal=Circulation | year= 1998 | volume= 98 | issue= 25 | pages= 2866-72 | pmid=9860789 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9860789 }} </ref> The definition of disease progression, however, may vary between individual studies.
*To date, there is no reliable information about the prevalence of [[secondary hypertension]] due to renal artery stenosis. Follow-up and prognosis for hypertensive patients with [[renal artery stenosis]] has not yet been achieved.

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]
[[Category: Needs content]]

Renal artery stenosis epidemiology and demographics

2020-12-12T22:21:54Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}}; {{AE}} {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==

[[Atherosclerotic renal artery stenosis]] (ARAS) is considered a disease of the elderly. The true prevalence of [[ARAS]] has not been reliably determined and [[prevalence]] rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Epidemiology and demographics==

[[Renal artery stenosis]] considered a disease of the elderly.<ref name="pmid11172181">{{cite journal| author=Safian RD, Textor SC| title=Renal-artery stenosis. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 6 | pages= 431-42 | pmid=11172181 | doi=10.1056/NEJM200102083440607 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11172181 }} </ref> It most commonly affects patients with cardiovascular co-morbidities, such as those with [[diabetes mellitus]], coronary and [[peripheral artery disease]], [[dyslipidemia]], [[essential hypertension]], and [[smoking]] history.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 |pages= 489-92 | pmid=2045754 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal functon changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>

*It is difficult to assess the real incidence and prevalence of renal artery stenosis because most patients with the disease are in fact asymptomatic.
*In one study that involved 14,152 patients undergoing [[abdominal aortography]], approximately 10% of the patients had [[Renal artery stenosis|RAS]] and 1.3% had bilateral [[Renal artery stenosis|RAS]], 60% of which were considered significant stenosis.<ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>
*Autopsy findings among 5194 patients between 1980 and 1988 showed that 4.3% of all patients [[Renal artery stenosis|RAS]], most of which were not diagnosed.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref> The frequency of RAS among patients with [[diabetes]] and [[hypertension]] was higher, reaching up to 10% of all patients. <ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
*Atherosclerotic [[renal artery stenosis]] affects approximately 0.5-7% of the U.S. population above the age of 65 years. It is present in almost 5% of patients with [[chronic kidney disease]].<ref name="pmid15954920">{{cite journal| author=Kalra PA, Guo H, Kausz AT, Gilbertson DT, Liu J, Chen SC et al.| title=Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 293-301 | pmid=15954920 | doi=10.1111/j.1523-1755.2005.00406.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954920 }} </ref><ref name="pmid12218965">{{cite journal| author=Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG et al.| title=Prevalence of renovascular disease in the elderly: a population-based study. | journal=J Vasc Surg | year= 2002 | volume= 36 | issue= 3 | pages= 443-51 | pmid=12218965 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12218965 }} </ref>
*Although stenosis may progress in 30-53% of patients within only 2-5 years. after diagnosis, only 3-15% of patient with [[Acute renal artery stenosis|ARAS]] progress to total occlusion of the [[renal arteries]].<ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal function changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg |year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9507221">{{cite journal| author=Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K et al.| title=Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. | journal=Kidney Int | year= 1998 | volume= 53 | issue= 3 | pages= 735-42 | pmid=9507221 | doi=10.1046/j.1523-1755.1998.00805.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9507221 }} </ref><ref name="pmid9860789">{{cite journal| author=Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ et al.| title=Prospective study of atherosclerotic disease progression in the renal artery. | journal=Circulation | year= 1998 | volume= 98 | issue= 25 | pages= 2866-72 | pmid=9860789 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9860789 }} </ref> The definition of disease progression, however, may vary between individual studies.
*To date, there is no reliable information about the prevalence of [[secondary hypertension]] due to renal artery stenosis. Follow-up and prognosis for hypertensive patients with [[renal artery stenosis]] has not yet been achieved.

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]
[[Category: Needs content]]

Renal artery stenosis causes

2020-12-12T21:52:58Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

[[Renal artery stenosis]] is most commonly caused by the development of [[atherosclerotic]] [[plaque]] in the [[renal arteries]] (termed atherosclerotic renal artery stenosis). Less frequently, it is caused by [[fibromuscular dysplasia]].

==Causes==

Unilateral [[Renal artery stenosis]] has two major causes:

1) Atherosclerosis<ref name="urlRenal artery stenosis - Symptoms and causes - Mayo Clinic">{{cite web |url=https://www.mayoclinic.org/diseases-conditions/renal-artery-stenosis/symptoms-causes/syc-20352777 |title=Renal artery stenosis - Symptoms and causes - Mayo Clinic |format= |work= |accessdate=}}</ref>: Most common cause seen in almost 60-90 percent of the cases associated with [[renal artery stenosis]]. [[Atherosclerosis]] mostly affects men over the age of 45 years and mainly involves the proximal part of the main [[renal artery]]. Although this condition is also commonly seen as an isolated lesion even in patients not having the underlying [[atherosclerotic]] [[disease]]. The [[risk factors]] associated with [[atherosclerosis]] are [[dyslipidemia]], [[cigarette smoking]], [[virus]] [[infection]], [[immune]] damage, and elevated concentrations of [[homocysteine]].

2) Fibromuscular dysplasia<ref name="pmid28613469">{{cite journal |vauthors=Bokhari MR, Bokhari SRA |title= |journal= |volume= |issue= |pages= |date= |pmid=28613469 |doi= |url=}}</ref><ref name="urlRenal Artery Stenosis - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK430718/#article-28335.s2 |title=Renal Artery Stenosis - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref>: This is responsible for causing [[renal artery stenosis]] in the remaining 10-30 percent of cases. This is most commonly seen in women under the age of 50 years and mainly involves middle and distal [[renal arteries]] and typically involves the middle and distal main [[renal artery]] or the [[intrarenal]] branches.

3) In, Less than 10 percent of the [[patient population]] other less common factors play a role like

- [[Thromboembolic]] [[disease]]

- [[Aortic aneurysm|Aortic aneurysms]]

- [[Takayasu arteritis]]

- [[Polyarteritis nodosa]]

- [[Retroperitoneal fibrosis]].

==References==
<references />

Renal artery stenosis pathophysiology

2020-12-12T21:48:55Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[Juxtaglomerular apparatus|juxtaglomerular apparatu]]<nowiki/>s through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the [[renin-angiotensin-aldosterone system]]<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to [[Angiotensin II]] with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

== Pathogenesis ==
[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the [[rarefaction]] of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]].

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis pathophysiology

2020-12-12T21:48:25Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[Juxtaglomerular apparatus|juxtaglomerular apparatu]]<nowiki/>s through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the [[renin-angiotensin-aldosterone system]]<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to [[Angiotensin II]] with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

 

== Pathogenesis ==
[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the [[rarefaction]] of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]].

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis pathophysiology

2020-12-12T21:45:26Z

Shivam Singla: /* Overview */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[Juxtaglomerular apparatus|juxtaglomerular apparatu]]<nowiki/>s through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the [[renin-angiotensin-aldosterone system]]<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to [[Angiotensin II]] with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the [[rarefaction]] of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]].

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis pathophysiology

2020-12-12T21:26:48Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in [[renal blood flow]] secondary to [[renal artery stenosis]] stimulates [[renin]] release from the [[juxtaglomerular]] apparatus through [[activation]] of the [[tubuloglomerular]] [[feedback]], [[baroreceptor]] [[reflex]], and the [[sympathetic nervous system]]. Elevated [[angiotensin II]] activities in turn cause elevation of the [[arterial]] pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and [[left ventricular hypertrophy]] and [[remodeling]].

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The [[blood flow]] to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the renin-angiotensin-aldosterone system<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to Angiotensin II with the help of ACE
*This [[angiotensin II]] directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of [[sodium]] and [[water]] thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged [[hypo-perfusion]] to the [[kidneys]] resulting in chronic stimulation and [[hyperplasia]] of the [[juxtaglomerular apparatus]]. This prolonged [[ischemia]] further leads to [[renal insufficiency]] and in turn [[progressive renal atrophy]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] [[perfusion]] drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in [[GFR]] is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] [[perfusion pressure]] by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant [[stenosis]] around 70-80%, there is the development of apparent [[cortical hypoxia]] and this [[hypoxia]] further leads to the rarefaction of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and [[restoration]] of [[blood flow]] to the [[kidneys]] will not help in getting back the [[kidney]] [[functions]].

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis epidemiology and demographics

2020-12-12T21:14:56Z

Shivam Singla: /* Epidemiology and demographics */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}}; {{AE}} {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==

Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly. The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Epidemiology and demographics==

[[Renal artery stenosis]] considered a disease of the elderly.<ref name="pmid11172181">{{cite journal| author=Safian RD, Textor SC| title=Renal-artery stenosis. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 6 | pages= 431-42 | pmid=11172181 | doi=10.1056/NEJM200102083440607 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11172181 }} </ref> It most commonly affects patients with cardiovascular co-morbidities, such as those with [[diabetes mellitus]], coronary and [[peripheral artery disease]], [[dyslipidemia]], [[essential hypertension]], and [[smoking]] history.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 |pages= 489-92 | pmid=2045754 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal functon changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>

*It is difficult to assess the real incidence and prevalence of renal artery stenosis because most patients with the disease are in fact asymptomatic.
*In one study that involved 14,152 patients undergoing abdominal aortography, approximately 10% of the patients had RAS and 1.3% had bilateral RAS, 60% of which were considered significant stenosis.<ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>
*Autopsy findings among 5194 patients between 1980 and 1988 showed that 4.3% of all patients RAS, most of which were not diagnosed.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref> The frequency of RAS among patients with [[diabetes]] and [[hypertension]] was higher, reaching up to 10% of all patients. <ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
*Atherosclerotic renal artery stenosis affects approximately 0.5-7% of the U.S. population above the age of 65 years. It is present in almost 5% of patients with [[chronic kidney disease]].<ref name="pmid15954920">{{cite journal| author=Kalra PA, Guo H, Kausz AT, Gilbertson DT, Liu J, Chen SC et al.| title=Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 293-301 | pmid=15954920 | doi=10.1111/j.1523-1755.2005.00406.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954920 }} </ref><ref name="pmid12218965">{{cite journal| author=Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG et al.| title=Prevalence of renovascular disease in the elderly: a population-based study. | journal=J Vasc Surg | year= 2002 | volume= 36 | issue= 3 | pages= 443-51 | pmid=12218965 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12218965 }} </ref>
*Although stenosis may progress in 30-53% of patients within only 2-5 years. after diagnosis, only 3-15% of patient with ARAS progress to total occlusion of the [[renal arteries]].<ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal function changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg |year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9507221">{{cite journal| author=Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K et al.| title=Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. | journal=Kidney Int | year= 1998 | volume= 53 | issue= 3 | pages= 735-42 | pmid=9507221 | doi=10.1046/j.1523-1755.1998.00805.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9507221 }} </ref><ref name="pmid9860789">{{cite journal| author=Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ et al.| title=Prospective study of atherosclerotic disease progression in the renal artery. | journal=Circulation | year= 1998 | volume= 98 | issue= 25 | pages= 2866-72 | pmid=9860789 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9860789 }} </ref> The definition of disease progression, however, may vary between individual studies.
*To date, there is no reliable information about the prevalence of [[secondary hypertension]] due to renal artery stenosis. Follow-up and prognosis for hypertensive patients with renal artery stenosis has not yet been achieved.

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]
[[Category: Needs content]]

Renal artery stenosis epidemiology and demographics

2020-12-12T21:13:01Z

Shivam Singla: /* Epidemiology and demographics */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}}; {{AE}} {{Shivam Singla}} [[User:YazanDaaboul|Yazan Daaboul]], [[User:Sergekorjian|Serge Korjian]]

==Overview==

Atherosclerotic renal artery stenosis (ARAS) is considered a disease of the elderly. The true prevalence of ARAS has not been reliably determined and prevalence rates present so far may in fact be an underestimate or an overestimate of the true prevalence due to selection criteria in different studies. The prevalence of ARAS increases substantially among patients with cardiovascular co-morbidities, such as [[diabetes mellitus]], [[dyslipidemia]], [[essential hypertension]], and known coronary or [[peripheral artery disease]].

==Epidemiology and demographics==

[[Renal artery stenosis]] considered a disease of the elderly.<ref name="pmid11172181">{{cite journal| author=Safian RD, Textor SC| title=Renal-artery stenosis. | journal=N Engl J Med | year= 2001 | volume= 344 | issue= 6 | pages= 431-42 | pmid=11172181 | doi=10.1056/NEJM200102083440607 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11172181 }} </ref> It most commonly affects patients with cardiovascular co-morbidities, such as those with [[diabetes mellitus]], coronary and [[peripheral artery disease]], [[dyslipidemia]], [[essential hypertension]], and [[smoking]] history.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 |pages= 489-92 | pmid=2045754 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal functon changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>

* It is difficult to assess the real incidence and prevalence of renal artery stenosis because most patients with the disease are in fact asymptomatic.
* Additionally, much controversy regarding the studies that examined the prevalence of ARAS and their methodology and inclusion criteria for mostly enrolling only those with cardiovascular risk factors.<ref name="pmid12466310">{{cite journal| author=Zoccali C, Mallamaci F, Finocchiaro P| title=Atherosclerotic renal artery stenosis: epidemiology, cardiovascular outcomes, and clinical prediction rules. | journal=J Am Soc Nephrol | year= 2002 | volume= 13 Suppl 3 | issue= | pages= S179-83 | pmid=12466310 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12466310 }} </ref>
* As such, the disease prevalence may thus be underestimated or overestimated.<ref name="pmid19907044">{{cite journal| author=Dworkin LD, Cooper CJ| title=Clinical practice. Renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1972-8 | pmid=19907044 | doi=10.1056/NEJMcp0809200 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907044 }} </ref>
* In one study that involved 14,152 patients undergoing abdominal aortography, approximately 10% of the patients had RAS and 1.3% had bilateral RAS, 60% of which were considered significant stenosis.<ref name="pmid9812088">{{cite journal| author=Crowley JJ, Santos RM, Peter RH, Puma JA, Schwab SJ, Phillips HR et al.| title=Progression of renal artery stenosis in patients undergoing cardiac catheterization. | journal=Am Heart J | year= 1998 | volume= 136 | issue= 5 | pages= 913-8 | pmid=9812088 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9812088 }} </ref>
* Autopsy findings among 5194 patients between 1980 and 1988 showed that 4.3% of all patients RAS, most of which were not diagnosed.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref> The frequency of RAS among patients with [[diabetes]] and [[hypertension]] was higher, reaching up to 10% of all patients. <ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
* Bilateral renal artery stenosis was higher in diabetic patients, but significant association was not reached in the study.<ref name="pmid2045754">{{cite journal| author=Sawicki PT, Kaiser S, Heinemann L, Frenzel H, Berger M| title=Prevalence of renal artery stenosis in diabetes mellitus--an autopsy study. | journal=J Intern Med | year= 1991 | volume= 229 | issue= 6 | pages= 489-92 | pmid=2045754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2045754 }} </ref>
* Atherosclerotic renal artery stenosis affects approximately 0.5-7% of the U.S. population above the age of 65 years. It is present in almost 5% of patients with [[chronic kidney disease]].<ref name="pmid15954920">{{cite journal| author=Kalra PA, Guo H, Kausz AT, Gilbertson DT, Liu J, Chen SC et al.| title=Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 293-301 | pmid=15954920 | doi=10.1111/j.1523-1755.2005.00406.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954920 }} </ref><ref name="pmid12218965">{{cite journal| author=Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG et al.| title=Prevalence of renovascular disease in the elderly: a population-based study. | journal=J Vasc Surg | year= 2002 | volume= 36 | issue= 3 | pages= 443-51 | pmid=12218965 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12218965 }} </ref>
* Although stenosis may progress in 30-53% of patients within only 2-5 years. after diagnosis, only 3-15% of patient with ARAS progress to total occlusion of the [[renal arteries]].<ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg | year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid7305653">{{cite journal| author=Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW et al.| title=Renovascular hypertension: anatomic and renal function changes during drug therapy. | journal=Arch Surg | year= 1981 | volume= 116 | issue= 11 | pages= 1408-15 | pmid=7305653 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7305653 }} </ref><ref name="pmid1880841">{{cite journal| author=Tollefson DF, Ernst CB| title=Natural history of atherosclerotic renal artery stenosis associated with aortic disease. | journal=J Vasc Surg |year= 1991 | volume= 14 | issue= 3 | pages= 327-31 | pmid=1880841 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1880841 }} </ref><ref name="pmid9507221">{{cite journal| author=Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K et al.| title=Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. | journal=Kidney Int | year= 1998 | volume= 53 | issue= 3 | pages= 735-42 | pmid=9507221 | doi=10.1046/j.1523-1755.1998.00805.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9507221 }} </ref><ref name="pmid9860789">{{cite journal| author=Caps MT, Perissinotto C, Zierler RE, Polissar NL, Bergelin RO, Tullis MJ et al.| title=Prospective study of atherosclerotic disease progression in the renal artery. | journal=Circulation | year= 1998 | volume= 98 | issue= 25 | pages= 2866-72 | pmid=9860789 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9860789 }} </ref> The definition of disease progression, however, may vary between individual studies.

To date, there is no reliable information about the prevalence of [[secondary hypertension]] due to renal artery stenosis. Follow-up and prognosis for hypertensive patients with renal artery stenosis has not yet been achieved.

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]
[[Category: Needs content]]

Renal artery stenosis causes

2020-12-12T21:10:53Z

Shivam Singla: /* Causes */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

Renal artery stenosis is most commonly caused by the development of atherosclerotic [[plaque]] in the renal arteries (termed atherosclerotic renal artery stenosis). Less frequently, it is caused by [[fibromuscular dysplasia]].

==Causes==

Unilateral [[Renal artery stenosis]] has two major causes:

1) Atherosclerosis<ref name="urlRenal artery stenosis - Symptoms and causes - Mayo Clinic">{{cite web |url=https://www.mayoclinic.org/diseases-conditions/renal-artery-stenosis/symptoms-causes/syc-20352777 |title=Renal artery stenosis - Symptoms and causes - Mayo Clinic |format= |work= |accessdate=}}</ref>: Most common cause seen in almost 60-90 percent of the cases associated with [[renal artery stenosis]]. [[Atherosclerosis]] mostly affects men over the age of 45 years and mainly involves the proximal part of the main [[renal artery]]. Although this condition is also commonly seen as an isolated lesion even in patients not having the underlying [[atherosclerotic]] [[disease]]. The [[risk factors]] associated with [[atherosclerosis]] are [[dyslipidemia]], [[cigarette smoking]], [[virus]] [[infection]], [[immune]] damage, and elevated concentrations of [[homocysteine]].

2) Fibromuscular dysplasia<ref name="pmid28613469">{{cite journal |vauthors=Bokhari MR, Bokhari SRA |title= |journal= |volume= |issue= |pages= |date= |pmid=28613469 |doi= |url=}}</ref><ref name="urlRenal Artery Stenosis - StatPearls - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK430718/#article-28335.s2 |title=Renal Artery Stenosis - StatPearls - NCBI Bookshelf |format= |work= |accessdate=}}</ref>: This is responsible for causing [[renal artery stenosis]] in the remaining 10-30 percent of cases. This is most commonly seen in women under the age of 50 years and mainly involves middle and distal [[renal arteries]] and typically involves the middle and distal main [[renal artery]] or the [[intrarenal]] branches.

3) In, Less than 10 percent of the patient population other less common factors play a role like

- [[Thromboembolic]] [[disease]]

- [[Aortic aneurysm|Aortic aneurysms]]

- [[Takayasu arteritis]]

- [[Polyarteritis nodosa]]

- [[Retroperitoneal fibrosis]].

==References==
<references />

Renal artery stenosis pathophysiology

2020-12-12T21:04:15Z

Shivam Singla: /* Pathophysiology */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in renal blood flow secondary to renal artery stenosis stimulates [[renin]] release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor]] reflex, and the sympathetic nervous system. Elevated [[angiotensin II]] activities in turn cause elevation of the arterial pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and left ventricular hypertrophy and remodeling.

==Pathophysiology==

*[[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
*The blood flow to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]].
*In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the renin-angiotensin-aldosterone system<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
*Renin converts angiotensinogen to angiotensin I and then further gets converted to Angiotensin II with the help of ACE
*This angiotensin II directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of sodium and water thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
*Prolonged hypo-perfusion to the kidneys resulting in chronic stimulation and hyperplasia of the juxtaglomerular apparatus. This prolonged ischemia further leads to renal insufficiency and in turn progressive renal atrophy<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] perfusion drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in GFR is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] perfusion pressure by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant stenosis around 70-80%, there is the development of apparent [[cortical hypoxia]] and this hypoxia further leads to the rarefaction of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and restoration of [[blood flow]] to the [[kidneys]] will not help in getting back the kidney functions.

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis pathophysiology

2020-12-12T21:01:53Z

Shivam Singla: /* Pathophysiology */

__NOTOC__
{{Renal artery stenosis}}

{{CMG}} {{AE}} {{Shivam Singla}}

==Overview==

The reduction in renal blood flow secondary to renal artery stenosis stimulates [[renin]] release from the juxtaglomerular apparatus through activation of the tubuloglomerular feedback, [[baroreceptor]] reflex, and the sympathetic nervous system. Elevated [[angiotensin II]] activities in turn cause elevation of the arterial pressure and other effects including [[aldosterone]] secretion, [[sodium]] retention, and left ventricular hypertrophy and remodeling.

==Pathophysiology==

* [[Renal artery stenosis]] means the narrowing of both [[renal]] [[arteries]] leading to the obstruction of [[blood flow]] and resulting in the stimulation of [[RAAS]].
* The blood flow to the [[kidneys]] is generally greater than perfusion to any other [[organ]] and the [[GFR]] mainly depends on the [[glomerular capillary hydrostatic pressure]]. In patients with [[RAS]], the reduced [[blood]] flow to the [[kidneys]] leads to the formation of [[collateral blood vessels]] and increases secretion of [[renin]] by juxtaglomerular apparatus<ref name="pmid19219002">{{cite journal |vauthors=Gomez RA, Sequeira Lopez ML |title=Who and where is the renal baroreceptor?: the connexin hypothesis |journal=Kidney Int |volume=75 |issue=5 |pages=460–2 |date=March 2009 |pmid=19219002 |pmc=3025775 |doi=10.1038/ki.2008.536 |url=}}</ref>and activation of the renin-angiotensin-aldosterone system<ref name="Garovic-2005">{{Cite journal | last1 = Garovic | first1 = VD. | last2 = Textor | first2 = SC. | title = Renovascular hypertension and ischemic nephropathy. | journal = Circulation | volume = 112 | issue = 9 | pages = 1362-74 | month = Aug | year = 2005 | doi = 10.1161/CIRCULATIONAHA.104.492348 | PMID = 16129817 }}</ref>
* Renin converts angiotensinogen to angiotensin I and then with the help of the enzyme [[ACE]] that is an angiotensin-converting enzyme it further gets converted to [[angiotensin II]].
* This angiotensin II directly causes [[vasoconstriction]] and also increases [[aldosterone]] which results in the retention of sodium and water thus leads to the development of [[renovascular hypertension]] that is also called [[secondary hypertension]].
* Prolonged hypo-perfusion to the kidneys resulting in chronic stimulation and hyperplasia of the juxtaglomerular apparatus. This prolonged ischemia further leads to renal insufficiency and in turn progressive renal atrophy<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>.

[[Glomerular filtration rate]] (GFR) is auto-regulated with the help of [[angiotensin II]] and numerous other modulators. The [[GFR]] gets affected when the [[renal]] perfusion drops below 70 mmHg<ref name="urlRenal Artery Stenosis | NIDDK">{{cite web |url=https://www.niddk.nih.gov/health-information/kidney-disease/renal-artery-stenosis#rasrvh |title=Renal Artery Stenosis | NIDDK |format= |work= |accessdate=}}</ref>. the apparent change in GFR is observed once the [[arterial]] lumen narrows by more than 50%. Numerous studies reported that [[GFR]] is reduced when altogether there is a reduction in [[renal]] perfusion pressure by more than 40% and a reduction in mean [[renal blood flow]] by 30%. However, even after this, the [[kidneys]] cortex and [[medulla]] can adapt without the development of severe [[hypoxia]]. So early disease can be managed with the medical approach and that can prevent the development of progressive function loss and [[fibrosis]]. But in cases with more significant stenosis around 70-80%, there is the development of apparent [[cortical hypoxia]] and this hypoxia further leads to the rarefaction of [[microvessels]] and ultimately leads to the development of [[interstitial fibrosis]]<ref name="pmid15284283">{{cite journal |vauthors=Textor SC |title=Ischemic nephropathy: where are we now? |journal=J Am Soc Nephrol |volume=15 |issue=8 |pages=1974–82 |date=August 2004 |pmid=15284283 |doi=10.1097/01.ASN.0000133699.97353.24 |url=}}</ref>. Therefore the loss of [[renal]] function and progressive [[renal disease]]. Eventually, it becomes irreversible and restoration of [[blood flow]] to the [[kidneys]] will not help in getting back the kidney functions.

[[Image:Renal artery stenosis diagram 001.gif|200px|Illustration of renal artery stenosis]]

==References==
{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

Renal artery stenosis angioplasty and stenting

2020-12-12T20:59:44Z

Shivam Singla: /* Indications for Renal Angioplasty or Stenting */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
[[Randomized controlled trials]] such as [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) and [[CORAL]] have not demonstrated a benefit of percutaneous [[revascularization]] over medical therapy among [[patients]] with [[unilateral]] [[renal artery stenosis]] (RAS). These [[trials]] have been criticized, however, because they did not enroll those [[patients]] who in observational data derived the greatest benefit, namely those [[patients]] who have a short duration of [[hypertension]], patients who are resistant to [[medical therapy]] for [[hypertension]], and [[patients]] who have recurrent flash [[pulmonary edema]]. For instance, in the [[ASTRAL]] trial, [[patients]] had [[hypertension]] for 5 years. Likewise, the mean number of [[antihypertensive]] agents was only 2.1 in the [[CORAL]] trial, and [[patients]] who were recently hospitalized with [[congestive heart failure]] were excluded from the [[CORAL trial]].

==Landmark Studies==
===ASTRAL Trial===

*The 2009 [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) trial was an unblinded trial that randomized 806 patients with [[RAS]] for 5 years to either [[revascularization]] and medical therapy or medical therapy alone in a 1:1 ratio.

*[[Angioplasty|Renal angioplasty]] was associated with significant risk and very little benefit in [[ASTRAL]].<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

*The rate of increase in [[creatinine]] was better among patients who underwent revascularization at -0.07x10-3 L/mmol/year vs -0.13x10-3 L/mmol/year among those treated with medical therapy.

*Similarly, the mean serum [[creatinine]] was lower in the revascularization group; but the number of renal events was similar. Nonetheless, the reduction in [[blood pressure]] was better with medical therapy.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref> Furthermore, cardiovascular events and death were not significantly different; but the rates of serious complications during [[revascularization]] were high, involving 23 patients and including 2 deaths and 3 amputations.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

===CORAL Trial===

*In the 2013 [[CORAL]] trial, 947 patients with [[atherosclerotic]] [[renal-artery stenosis]] who had either [[chronic kidney disease]] or persistent [[systolic hypertension]] on > or = to 2 [[antihypertensive drugs]] were randomized to either [[renal-artery stenting]] + [[medical therapy]] or medical therapy alone.

*After a median follow-up of 43 months, the primary endpoint (the composite of either death from cardiovascular or renal causes, [[myocardial infarction]], [[stroke]], hospitalization for [[congestive heart failure]], progressive [[renal insufficiency]], or the need for renal-replacement therapy) did not differ between the strategies: 35.1% and 35.8%; 0.94; 95% confidence interval [CI], 0.76 to 1.17; P=0.58, for stenting + medical therapy vs medical therapy alone); nor did any of the components of the primary endpoint (including mortality).

*There was a modest benefit in [[systolic blood pressure]] reduction in the stented group (−2.3 mm Hg; 95% CI, −4.4 to −0.2; P=0.03).

 

== Indications for Renal Angioplasty or Stenting ==
Based upon the modest data observed in the above [[observational]] studies, the following are considered reasonable indications for [[percutaneous intervention]]:<ref name="pmid24074824">{{cite journal| author=Ritchie J, Green D, Chrysochou C, Chalmers N, Foley RN, Kalra PA| title=High-risk clinical presentations in atherosclerotic renovascular disease: prognosis and response to renal artery revascularization. | journal=Am J Kidney Dis | year= 2014 | volume= 63 | issue= 2 | pages= 186-97 | pmid=24074824 | doi=10.1053/j.ajkd.2013.07.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24074824 }} </ref><ref name="pmid19937777">{{cite journal| author=Kalra PA, Chrysochou C, Green D, Cheung CM, Khavandi K, Sixt S et al.| title=The benefit of renal artery stenting in patients with atheromatous renovascular disease and advanced chronic kidney disease. | journal=Catheter Cardiovasc Interv | year= 2010 | volume= 75 | issue= 1 | pages= 1-10 | pmid=19937777 | doi=10.1002/ccd.22290 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19937777 }} </ref> <ref name="pmid12710843">{{cite journal| author=Gray BH, Olin JW, Childs MB, Sullivan TM, Bacharach JM| title=Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. | journal=Vasc Med | year= 2002 | volume= 7 | issue= 4 | pages= 275-9 | pmid=12710843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12710843 }} </ref>

*Failure of [[medical therapy]] with [[persistent hypertension]] or a decline in [[renal]] function while on medical therapy
**[[Revascularization]] was recommended by ACC/AHA guidelines, with class B evidence, in [[hypertensive]] [[patients]] who have hemodynamically significant [[RAS]], [[malignant hypertension]], [[resistant hypertension]], and/or accelerated [[hypertension]], and among those with unexplained [[unilateral]] [[small kidneys]] or intolerance to anti-[[hypertensive]] [[medications]].<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of [[patients]] with [[peripheral artery disease]] (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>

*Refractory [[heart failure]] and or recurrent [[flash pulmonary edema]]
**[[Revascularization]] was indicated at level B evidence in [[patients]] with [[thermodynamically]] significant [[RAS]] and [[recurrent]] [[congestive heart failure]] of undefined cause or in cases of sudden [[flash pulmonary edema]] with unexplained etiology, as well as for [[unstable angina]].<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>
*Brief duration of [[hypertension]] preceding the diagnosis of [[renal artery stenosis]]

 

==Management of Patients With Peripheral Artery Disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines<ref name="pmid23473760">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2013 | volume= 61 | issue= 14 | pages= 1555-70 | pmid=23473760 | doi=10.1016/j.jacc.2013.01.004 | pmc=4492473 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23473760 }} </ref>==
{| class="wikitable"
|+
!Indications for Revascularization of Asymptomatic Stenosis
![[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|Class IIb]]
<nowiki>"</nowiki>'''1.''' Percutaneous revascularization may be considered for the treatment of an asymptomatic bilateral or a solitary viable kidney with a hemodynamically significant RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''2.''' The usefulness of percutaneous revascularization of an asymptomatic unilateral hemodynamically significant RAS in a viable kidney is not well established and is presently clinically unproven. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
 
|-
|'''Hypertension'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and accelerated hypertension, [[resistant hypertension]], [[malignant hypertension]], [[hypertension]] with an unexplained unilateral small kidney, and hypertension with intolerance to medication. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|-
|'''Preservation of Renal'''
'''Function'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with RAS and progressive [[chronic kidney disease]] with bilateral RAS or a RAS to a solitary functioning kidney. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIb''']]

'''"1. Percutaneous revascularization may be considered for patients with RAS and [[chronic renal insufficiency]] with unilateral RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>'''
|-
|'''Impact of RAS on'''
'''Congestive Heart'''

'''Failure and Unstable'''

'''Angina'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Percutaneous revascularization is indicated for patients with hemodynamically significant RAS and recurrent, unexplained [[congestive heart failure]] or sudden, unexplained [[pulmonary edema]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]

'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and [[unstable angina]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
 
|-
|'''Endovascular'''
'''Treatment for RAS'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Renal stent placement is indicated for ostial atherosclerotic RAS lesions that meet the clinical criteria for intervention. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

'''"2. [[Balloon angioplasty]] with bail-out stent placement if necessary is recommended for [[fibromuscular dysplasia]] lesions. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|}

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

{{WH}}
{{WS}}

Renal artery stenosis angioplasty and stenting

2020-12-12T20:55:23Z

Shivam Singla: /* CORAL Trial */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
[[Randomized controlled trials]] such as [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) and [[CORAL]] have not demonstrated a benefit of percutaneous [[revascularization]] over medical therapy among [[patients]] with [[unilateral]] [[renal artery stenosis]] (RAS). These [[trials]] have been criticized, however, because they did not enroll those [[patients]] who in observational data derived the greatest benefit, namely those [[patients]] who have a short duration of [[hypertension]], patients who are resistant to [[medical therapy]] for [[hypertension]], and [[patients]] who have recurrent flash [[pulmonary edema]]. For instance, in the [[ASTRAL]] trial, [[patients]] had [[hypertension]] for 5 years. Likewise, the mean number of [[antihypertensive]] agents was only 2.1 in the [[CORAL]] trial, and [[patients]] who were recently hospitalized with [[congestive heart failure]] were excluded from the [[CORAL trial]].

==Landmark Studies==
===ASTRAL Trial===

*The 2009 [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) trial was an unblinded trial that randomized 806 patients with [[RAS]] for 5 years to either [[revascularization]] and medical therapy or medical therapy alone in a 1:1 ratio.

*[[Angioplasty|Renal angioplasty]] was associated with significant risk and very little benefit in [[ASTRAL]].<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

*The rate of increase in [[creatinine]] was better among patients who underwent revascularization at -0.07x10-3 L/mmol/year vs -0.13x10-3 L/mmol/year among those treated with medical therapy.

*Similarly, the mean serum [[creatinine]] was lower in the revascularization group; but the number of renal events was similar. Nonetheless, the reduction in [[blood pressure]] was better with medical therapy.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref> Furthermore, cardiovascular events and death were not significantly different; but the rates of serious complications during [[revascularization]] were high, involving 23 patients and including 2 deaths and 3 amputations.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

===CORAL Trial===

*In the 2013 [[CORAL]] trial, 947 patients with [[atherosclerotic]] [[renal-artery stenosis]] who had either [[chronic kidney disease]] or persistent [[systolic hypertension]] on > or = to 2 [[antihypertensive drugs]] were randomized to either [[renal-artery stenting]] + [[medical therapy]] or medical therapy alone.

*After a median follow-up of 43 months, the primary endpoint (the composite of either death from cardiovascular or renal causes, [[myocardial infarction]], [[stroke]], hospitalization for [[congestive heart failure]], progressive [[renal insufficiency]], or the need for renal-replacement therapy) did not differ between the strategies: 35.1% and 35.8%; 0.94; 95% confidence interval [CI], 0.76 to 1.17; P=0.58, for stenting + medical therapy vs medical therapy alone); nor did any of the components of the primary endpoint (including mortality).

*There was a modest benefit in [[systolic blood pressure]] reduction in the stented group (−2.3 mm Hg; 95% CI, −4.4 to −0.2; P=0.03).

 

== Indications for Renal Angioplasty or Stenting ==
Based upon the modest data observed in the above observational studies, the following are considered reasonable indications for percutaneous intervention:<ref name="pmid24074824">{{cite journal| author=Ritchie J, Green D, Chrysochou C, Chalmers N, Foley RN, Kalra PA| title=High-risk clinical presentations in atherosclerotic renovascular disease: prognosis and response to renal artery revascularization. | journal=Am J Kidney Dis | year= 2014 | volume= 63 | issue= 2 | pages= 186-97 | pmid=24074824 | doi=10.1053/j.ajkd.2013.07.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24074824 }} </ref><ref name="pmid19937777">{{cite journal| author=Kalra PA, Chrysochou C, Green D, Cheung CM, Khavandi K, Sixt S et al.| title=The benefit of renal artery stenting in patients with atheromatous renovascular disease and advanced chronic kidney disease. | journal=Catheter Cardiovasc Interv | year= 2010 | volume= 75 | issue= 1 | pages= 1-10 | pmid=19937777 | doi=10.1002/ccd.22290 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19937777 }} </ref> <ref name="pmid12710843">{{cite journal| author=Gray BH, Olin JW, Childs MB, Sullivan TM, Bacharach JM| title=Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. | journal=Vasc Med | year= 2002 | volume= 7 | issue= 4 | pages= 275-9 | pmid=12710843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12710843 }} </ref>

*Failure of medical therapy with persistent hypertension or a decline in renal function while on medical therapy
**Revascularization was recommended by ACC/AHA guidelines, with class B evidence, in hypertensive patients who have hemodynamically significant RAS, malignant, resistant, and/or accelerated [[hypertension]], and among those with unexplained unilateral small kidneys or intolerance to anti-hypertensive medications.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>

*Refractory heart failure and or recurrent flash pulmonary edema
**Revascularization was indicated at level B evidence in patients with hemodynamically significant RAS and recurrent [[congestive heart failure]] of undefined cause or in cases of sudden flash pulmonary edema with unexplained etiology, as well as for unstable angina.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>
*Brief duration of hypertension preceding diagnosis of renal artery stenosis

 
==Management of Patients With Peripheral Artery Disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines<ref name="pmid23473760">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2013 | volume= 61 | issue= 14 | pages= 1555-70 | pmid=23473760 | doi=10.1016/j.jacc.2013.01.004 | pmc=4492473 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23473760 }} </ref>==
{| class="wikitable"
|+
!Indications for Revascularization of Asymptomatic Stenosis
![[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|Class IIb]]
<nowiki>"</nowiki>'''1.''' Percutaneous revascularization may be considered for the treatment of an asymptomatic bilateral or a solitary viable kidney with a hemodynamically significant RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''2.''' The usefulness of percutaneous revascularization of an asymptomatic unilateral hemodynamically significant RAS in a viable kidney is not well established and is presently clinically unproven. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
 
|-
|'''Hypertension'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and accelerated hypertension, [[resistant hypertension]], [[malignant hypertension]], [[hypertension]] with an unexplained unilateral small kidney, and hypertension with intolerance to medication. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|-
|'''Preservation of Renal'''
'''Function'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with RAS and progressive [[chronic kidney disease]] with bilateral RAS or a RAS to a solitary functioning kidney. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIb''']]

'''"1. Percutaneous revascularization may be considered for patients with RAS and [[chronic renal insufficiency]] with unilateral RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>'''
|-
|'''Impact of RAS on'''
'''Congestive Heart'''

'''Failure and Unstable'''

'''Angina'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Percutaneous revascularization is indicated for patients with hemodynamically significant RAS and recurrent, unexplained [[congestive heart failure]] or sudden, unexplained [[pulmonary edema]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]

'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and [[unstable angina]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
 
|-
|'''Endovascular'''
'''Treatment for RAS'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Renal stent placement is indicated for ostial atherosclerotic RAS lesions that meet the clinical criteria for intervention. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

'''"2. [[Balloon angioplasty]] with bail-out stent placement if necessary is recommended for [[fibromuscular dysplasia]] lesions. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|}

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

{{WH}}
{{WS}}

Renal artery stenosis angioplasty and stenting

2020-12-12T20:54:40Z

Shivam Singla: /* Overview */

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
[[Randomized controlled trials]] such as [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) and [[CORAL]] have not demonstrated a benefit of percutaneous [[revascularization]] over medical therapy among [[patients]] with [[unilateral]] [[renal artery stenosis]] (RAS). These [[trials]] have been criticized, however, because they did not enroll those [[patients]] who in observational data derived the greatest benefit, namely those [[patients]] who have a short duration of [[hypertension]], patients who are resistant to [[medical therapy]] for [[hypertension]], and [[patients]] who have recurrent flash [[pulmonary edema]]. For instance, in the [[ASTRAL]] trial, [[patients]] had [[hypertension]] for 5 years. Likewise, the mean number of [[antihypertensive]] agents was only 2.1 in the [[CORAL]] trial, and [[patients]] who were recently hospitalized with [[congestive heart failure]] were excluded from the [[CORAL trial]].

==Landmark Studies==
===ASTRAL Trial===

*The 2009 [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) trial was an unblinded trial that randomized 806 patients with [[RAS]] for 5 years to either [[revascularization]] and medical therapy or medical therapy alone in a 1:1 ratio.

*[[Angioplasty|Renal angioplasty]] was associated with significant risk and very little benefit in [[ASTRAL]].<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

*The rate of increase in [[creatinine]] was better among patients who underwent revascularization at -0.07x10-3 L/mmol/year vs -0.13x10-3 L/mmol/year among those treated with medical therapy.

*Similarly, the mean serum [[creatinine]] was lower in the revascularization group; but the number of renal events was similar. Nonetheless, the reduction in [[blood pressure]] was better with medical therapy.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref> Furthermore, cardiovascular events and death were not significantly different; but the rates of serious complications during [[revascularization]] were high, involving 23 patients and including 2 deaths and 3 amputations.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

===CORAL Trial===

*In the 2013 CORAL trial, 947 patients with atherosclerotic [[renal-artery stenosis]] who had either [[chronic kidney disease]] or persistent [[systolic hypertension]] on > or = to 2 [[antihypertensive drugs]] were randomized to either renal-artery stenting + medical therapy or medical therapy alone.

*After a median follow-up of 43 months, the primary endpoint (the composite of either death from cardiovascular or renal causes, [[myocardial infarction]], [[stroke]], hospitalization for [[congestive heart failure]], progressive [[renal insufficiency]], or the need for renal-replacement therapy) did not differ between the strategies: 35.1% and 35.8%; 0.94; 95% confidence interval [CI], 0.76 to 1.17; P=0.58, for stenting + medical therapy vs medical therapy alone); nor did any of the components of the primary endpoint (including mortality).

*There was a modest benefit in [[systolic blood pressure]] reduction in the stented group (−2.3 mm Hg; 95% CI, −4.4 to −0.2; P=0.03).

 

== Indications for Renal Angioplasty or Stenting ==
Based upon the modest data observed in the above observational studies, the following are considered reasonable indications for percutaneous intervention:<ref name="pmid24074824">{{cite journal| author=Ritchie J, Green D, Chrysochou C, Chalmers N, Foley RN, Kalra PA| title=High-risk clinical presentations in atherosclerotic renovascular disease: prognosis and response to renal artery revascularization. | journal=Am J Kidney Dis | year= 2014 | volume= 63 | issue= 2 | pages= 186-97 | pmid=24074824 | doi=10.1053/j.ajkd.2013.07.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24074824 }} </ref><ref name="pmid19937777">{{cite journal| author=Kalra PA, Chrysochou C, Green D, Cheung CM, Khavandi K, Sixt S et al.| title=The benefit of renal artery stenting in patients with atheromatous renovascular disease and advanced chronic kidney disease. | journal=Catheter Cardiovasc Interv | year= 2010 | volume= 75 | issue= 1 | pages= 1-10 | pmid=19937777 | doi=10.1002/ccd.22290 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19937777 }} </ref> <ref name="pmid12710843">{{cite journal| author=Gray BH, Olin JW, Childs MB, Sullivan TM, Bacharach JM| title=Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. | journal=Vasc Med | year= 2002 | volume= 7 | issue= 4 | pages= 275-9 | pmid=12710843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12710843 }} </ref>

*Failure of medical therapy with persistent hypertension or a decline in renal function while on medical therapy
**Revascularization was recommended by ACC/AHA guidelines, with class B evidence, in hypertensive patients who have hemodynamically significant RAS, malignant, resistant, and/or accelerated [[hypertension]], and among those with unexplained unilateral small kidneys or intolerance to anti-hypertensive medications.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>

*Refractory heart failure and or recurrent flash pulmonary edema
**Revascularization was indicated at level B evidence in patients with hemodynamically significant RAS and recurrent [[congestive heart failure]] of undefined cause or in cases of sudden flash pulmonary edema with unexplained etiology, as well as for unstable angina.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>
*Brief duration of hypertension preceding diagnosis of renal artery stenosis

 
==Management of Patients With Peripheral Artery Disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines<ref name="pmid23473760">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2013 | volume= 61 | issue= 14 | pages= 1555-70 | pmid=23473760 | doi=10.1016/j.jacc.2013.01.004 | pmc=4492473 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23473760 }} </ref>==
{| class="wikitable"
|+
!Indications for Revascularization of Asymptomatic Stenosis
![[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|Class IIb]]
<nowiki>"</nowiki>'''1.''' Percutaneous revascularization may be considered for the treatment of an asymptomatic bilateral or a solitary viable kidney with a hemodynamically significant RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''2.''' The usefulness of percutaneous revascularization of an asymptomatic unilateral hemodynamically significant RAS in a viable kidney is not well established and is presently clinically unproven. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
 
|-
|'''Hypertension'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and accelerated hypertension, [[resistant hypertension]], [[malignant hypertension]], [[hypertension]] with an unexplained unilateral small kidney, and hypertension with intolerance to medication. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|-
|'''Preservation of Renal'''
'''Function'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with RAS and progressive [[chronic kidney disease]] with bilateral RAS or a RAS to a solitary functioning kidney. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIb''']]

'''"1. Percutaneous revascularization may be considered for patients with RAS and [[chronic renal insufficiency]] with unilateral RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>'''
|-
|'''Impact of RAS on'''
'''Congestive Heart'''

'''Failure and Unstable'''

'''Angina'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Percutaneous revascularization is indicated for patients with hemodynamically significant RAS and recurrent, unexplained [[congestive heart failure]] or sudden, unexplained [[pulmonary edema]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]

'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and [[unstable angina]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
 
|-
|'''Endovascular'''
'''Treatment for RAS'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Renal stent placement is indicated for ostial atherosclerotic RAS lesions that meet the clinical criteria for intervention. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

'''"2. [[Balloon angioplasty]] with bail-out stent placement if necessary is recommended for [[fibromuscular dysplasia]] lesions. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|}

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

{{WH}}
{{WS}}

Renal artery stenosis angioplasty and stenting

2020-12-12T20:31:19Z

Shivam Singla:

__NOTOC__
{{Renal artery stenosis}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

==Overview==
Randomized controlled trials such as ASTRAL (Angioplasty and Stenting for Renal Artery Lesions) and CORAL have not demonstrated a benefit of percutaneous revascularization over medical therapy among patients with unilateral [[renal artery stenosis]] (RAS). These trials have been criticized, however, because they did not enroll those patients who in observational data derived the greatest benefit, namely those patients who have a short duration of [[hypertension]], patients who are resistant to medical therapy for hypertension, and patients who have recurrent flash [[pulmonary edema]]. For instance, in the ASTRAL trial, patients had hypertension for 5 years. Likewise, the mean number of antihypertensive agents was only 2.1 in the CORAL trial, and patients who were recently hospitalized with [[congestive heart failure]] were excluded from the CORAL trial.

==Landmark Studies==
===ASTRAL Trial===

*The 2009 [[ASTRAL]] (Angioplasty and Stenting for Renal Artery Lesions) trial was an unblinded trial that randomized 806 patients with [[RAS]] for 5 years to either [[revascularization]] and medical therapy or medical therapy alone in a 1:1 ratio.

*[[Angioplasty|Renal angioplasty]] was associated with significant risk and very little benefit in [[ASTRAL]].<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

*The rate of increase in [[creatinine]] was better among patients who underwent revascularization at -0.07x10-3 L/mmol/year vs -0.13x10-3 L/mmol/year among those treated with medical therapy.

*Similarly, the mean serum [[creatinine]] was lower in the revascularization group; but the number of renal events was similar. Nonetheless, the reduction in [[blood pressure]] was better with medical therapy.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref> Furthermore, cardiovascular events and death were not significantly different; but the rates of serious complications during [[revascularization]] were high, involving 23 patients and including 2 deaths and 3 amputations.<ref name="pmid19907042">{{cite journal| author=ASTRAL Investigators. Wheatley K, Ives N, Gray R, Kalra PA, Moss JG et al.| title=Revascularization versus medical therapy for renal-artery stenosis. | journal=N Engl J Med | year= 2009 | volume= 361 | issue= 20 | pages= 1953-62 | pmid=19907042 | doi=10.1056/NEJMoa0905368 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19907042 }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20157130 Review in: Ann Intern Med. 2010 Feb 16;152(4):JC-26] </ref>

===CORAL Trial===

*In the 2013 CORAL trial, 947 patients with atherosclerotic [[renal-artery stenosis]] who had either [[chronic kidney disease]] or persistent [[systolic hypertension]] on > or = to 2 [[antihypertensive drugs]] were randomized to either renal-artery stenting + medical therapy or medical therapy alone.

*After a median follow-up of 43 months, the primary endpoint (the composite of either death from cardiovascular or renal causes, [[myocardial infarction]], [[stroke]], hospitalization for [[congestive heart failure]], progressive [[renal insufficiency]], or the need for renal-replacement therapy) did not differ between the strategies: 35.1% and 35.8%; 0.94; 95% confidence interval [CI], 0.76 to 1.17; P=0.58, for stenting + medical therapy vs medical therapy alone); nor did any of the components of the primary endpoint (including mortality).

*There was a modest benefit in [[systolic blood pressure]] reduction in the stented group (−2.3 mm Hg; 95% CI, −4.4 to −0.2; P=0.03).

 

== Indications for Renal Angioplasty or Stenting ==
Based upon the modest data observed in the above observational studies, the following are considered reasonable indications for percutaneous intervention:<ref name="pmid24074824">{{cite journal| author=Ritchie J, Green D, Chrysochou C, Chalmers N, Foley RN, Kalra PA| title=High-risk clinical presentations in atherosclerotic renovascular disease: prognosis and response to renal artery revascularization. | journal=Am J Kidney Dis | year= 2014 | volume= 63 | issue= 2 | pages= 186-97 | pmid=24074824 | doi=10.1053/j.ajkd.2013.07.020 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24074824 }} </ref><ref name="pmid19937777">{{cite journal| author=Kalra PA, Chrysochou C, Green D, Cheung CM, Khavandi K, Sixt S et al.| title=The benefit of renal artery stenting in patients with atheromatous renovascular disease and advanced chronic kidney disease. | journal=Catheter Cardiovasc Interv | year= 2010 | volume= 75 | issue= 1 | pages= 1-10 | pmid=19937777 | doi=10.1002/ccd.22290 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19937777 }} </ref> <ref name="pmid12710843">{{cite journal| author=Gray BH, Olin JW, Childs MB, Sullivan TM, Bacharach JM| title=Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. | journal=Vasc Med | year= 2002 | volume= 7 | issue= 4 | pages= 275-9 | pmid=12710843 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12710843 }} </ref>

*Failure of medical therapy with persistent hypertension or a decline in renal function while on medical therapy
**Revascularization was recommended by ACC/AHA guidelines, with class B evidence, in hypertensive patients who have hemodynamically significant RAS, malignant, resistant, and/or accelerated [[hypertension]], and among those with unexplained unilateral small kidneys or intolerance to anti-hypertensive medications.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>

*Refractory heart failure and or recurrent flash pulmonary edema
**Revascularization was indicated at level B evidence in patients with hemodynamically significant RAS and recurrent [[congestive heart failure]] of undefined cause or in cases of sudden flash pulmonary edema with unexplained etiology, as well as for unstable angina.<ref name="pmid23457117">{{cite journal| author=Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA guideline recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=Circulation | year= 2013 | volume= 127 | issue= 13 | pages= 1425-43 | pmid=23457117 | doi=10.1161/CIR.0b013e31828b82aa | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23457117 }} </ref>
*Brief duration of hypertension preceding diagnosis of renal artery stenosis

 
==Management of Patients With Peripheral Artery Disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines<ref name="pmid23473760">{{cite journal| author=Rooke TW, Hirsch AT, Misra S, Sidawy AN, Beckman JA, Findeiss L et al.| title=Management of patients with peripheral artery disease (compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2013 | volume= 61 | issue= 14 | pages= 1555-70 | pmid=23473760 | doi=10.1016/j.jacc.2013.01.004 | pmc=4492473 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23473760 }} </ref>==
{| class="wikitable"
|+
!Indications for Revascularization of Asymptomatic Stenosis
![[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|Class IIb]]
<nowiki>"</nowiki>'''1.''' Percutaneous revascularization may be considered for the treatment of an asymptomatic bilateral or a solitary viable kidney with a hemodynamically significant RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>

<nowiki>"</nowiki>'''2.''' The usefulness of percutaneous revascularization of an asymptomatic unilateral hemodynamically significant RAS in a viable kidney is not well established and is presently clinically unproven. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>
 
|-
|'''Hypertension'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and accelerated hypertension, [[resistant hypertension]], [[malignant hypertension]], [[hypertension]] with an unexplained unilateral small kidney, and hypertension with intolerance to medication. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|-
|'''Preservation of Renal'''
'''Function'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]
'''"1. Percutaneous revascularization is reasonable for patients with RAS and progressive [[chronic kidney disease]] with bilateral RAS or a RAS to a solitary functioning kidney. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIb''']]

'''"1. Percutaneous revascularization may be considered for patients with RAS and [[chronic renal insufficiency]] with unilateral RAS. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: C]])''<nowiki>"</nowiki>'''
|-
|'''Impact of RAS on'''
'''Congestive Heart'''

'''Failure and Unstable'''

'''Angina'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Percutaneous revascularization is indicated for patients with hemodynamically significant RAS and recurrent, unexplained [[congestive heart failure]] or sudden, unexplained [[pulmonary edema]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class IIa''']]

'''"1. Percutaneous revascularization is reasonable for patients with hemodynamically significant RAS and [[unstable angina]] (see text). ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
 
|-
|'''Endovascular'''
'''Treatment for RAS'''
|[[ACC AHA Guidelines Classification Scheme#Classification of Recommendations|'''Class I''']]
'''"1. Renal stent placement is indicated for ostial atherosclerotic RAS lesions that meet the clinical criteria for intervention. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''

'''"2. [[Balloon angioplasty]] with bail-out stent placement if necessary is recommended for [[fibromuscular dysplasia]] lesions. ''([[ACC AHA Guidelines Classification Scheme#Level of Evidence|Level of Evidence: B]])''<nowiki>"</nowiki>'''
|}

==References==

{{Reflist|2}}

[[Category:Kidney diseases]]
[[Category:Nephrology]]
[[Category:Cardiology]]

{{WH}}
{{WS}}

Renal artery stenosis medical therapy

2020-12-12T20:25:27Z

Shivam Singla: /* Surgery */

__NOTOC__

{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

{{Renal artery stenosis}}

==Overview==
Patients with [[Renal artery stenosis]] require the widespread use of intensive [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in [[renal]] function after using the [[ACE inhibitors]] and [[ARB]], but it is neither a sensitive nor specific finding. Aggressive [[statin]] use, optimal [[glycemic]] regulation, and therapy for [[smoking]] abstinence are of vital significance. Other modalities used are [[renal artery]] [[revascularization]], [[Percutaneous transluminal renal angioplasty]], [[Renal artery stenting]], [[brachytherapy]] and cutting [[balloon atherotomy]], and [[surgery]] in complicated and nonresponding cases. Although [[morbidity]] and [[mortality]] are higher associated with [[surgery]] as compared to stenting.

==Treatment==

===Medical Therapy===
Patients with [[Renal artery stenosis]] require the widespread use of [[intensive]] [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in the [[renal function]] after using the [[ACE inhibitors]] and [[ARB]], but it is neither sensitive nor specific<ref name="pmid6337327">{{cite journal |vauthors=Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ |title=Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney |journal=N Engl J Med |volume=308 |issue=7 |pages=373–6 |date=February 1983 |pmid=6337327 |doi=10.1056/NEJM198302173080706 |url=}}</ref>. Aggressive [[statin]] use, optimal [[glycemic regulation]], and therapy for [[smoking]] abstinence are of vital significance.

Aggressive use of [[statins]], optimal [[glycemic control]], and [[smoking]] cessation counseling is of paramount importance. The results of various medical regimens on the treatment of [[ARAS]]-related [[hypertension]] were not analyzed in a [[randomized clinical trial]] because such [[patients]] frequently have [[refractory]] [[hypertension]] and need multiple [[antihypertensive]] [[medicines]]. [[Medical therapy]] is preferred for [[revascularization]] in [[patients]] with [[ARAS]] and progressive [[renal disease]] (i.e. chronic renal dysfunction, proteinuria[>1 g/d]), diffuse [[intrarenal vascular disease]], and [[renal atrophy]]<ref name="pmid15580159">{{cite journal |vauthors=Bokhari SW, Faxon DP |title=Current advances in the diagnosis and treatment of renal artery stenosis |journal=Rev Cardiovasc Med |volume=5 |issue=4 |pages=204–15 |date=2004 |pmid=15580159 |doi= |url=}}</ref>.

===Renal Artery Revascularization===
It is less obvious and much more contentious whether [[patients]] with [[ARAS]] and [[hypertension]] would undergo [[surgical revascularization]]. According to studies [[patients]] with extreme [[ostial]] [[renal artery stenosis]] who have been successfully [[revascularized]] [[percutaneously]] do not necessarily have therapeutic benefits.

The ACC/AHA description of [[RAS]] is as follows:

(1) visually approximate [[stenosis]] of 50 percent to 70 percent diameter with a translational peak gradient of at least 20 mm Hg or a mean gradient of at least 10 mm Hg

(2) [[angiographic stenosis]] of at least 70 percent diameter

(3) greater than 70% stenosis according to the measurement by [[intravascular ultrasounds]]<ref name="pmid8178389">{{cite journal |vauthors=Olin JW |title=Role of duplex ultrasonography in screening for significant renal artery disease |journal=Urol Clin North Am |volume=21 |issue=2 |pages=215–26 |date=May 1994 |pmid=8178389 |doi= |url=}}</ref>.

Present ACC/AHA recommendations do not, however, include these steps and prescribe [[revascularization]] of [[ARAS]] only when it is associated with certain [[medical conditions]] mentioned as follows:

1) Asymptomatic [[stenosis]]: [[Percutaneous revascularization]] can be considered for the treatment of:

*An asymptomatic bilateral

*Solitary viable [[kidney]] with [[thermodynamically]] significant [[ARAS]] (class Jib, degree of proof II.OF.I C),.

*The efficacy of [[percutaneous]] or asymptomatic unilateral hemodynamically significant [[ARAS]] in a viable kidney is not well known and clinically unrecognized (class 11b, LOE C)

2) [[Hypertension]]

*[[Percutaneous revascularization]] is used for patients with
*Hemodynamically significant [[renal artery stenosis]] along with accelerated [[hypertension]]
*[[Malignant hypertension]]
*[[Resistant hypertension]]
*In cases with [[hypertension]] and associated [[unilateral small kidney]].

3) Preservation of [[renal function]]

*[[Percutaneous revascularization]] is helpful in patients with [[ARAS]] + [[Chronic progressive kidney disease]] with [[bilateral renal artery stenosis]] or solitary functioning [[kidney]]. (Class IIa, LOE B)

*Also considered significant in [[patients]] with [[RAS]] and [[chronic renal insufficiency]] with [[unilateral renal artery stenosis]]. (Class IIb, LOE C)

4) Effects of [[renal artery stenosis]] on [[Congestive heart failure]] and [[unstable angina]]: [[Percutaneous revascularization]] is considered in [[patients]] with

*[[RAS]] + Recurrent [[congestive heart failure]] or sudden unexplained [[pulmonary edema]]. (Class I, LOE B)
*[[Patients]] with hemodynamically significant [[RAS]] along with [[unstable angina]] (Class IIa, LOE B)

 

===Percutaneous Transluminal Renal Angioplasty===
*Dutch [[Renal Artery Stenosis]] Intervention Cooperative (DRASTIC)<ref name="pmid10749962">{{cite journal |vauthors=van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in 't Veld AJ, Schalekamp MA |title=The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group |journal=N Engl J Med |volume=342 |issue=14 |pages=1007–14 |date=April 2000 |pmid=10749962 |doi=10.1056/NEJM200004063421403 |url=}}</ref> did a study to compare the effects of [[drug treatment]] and [[PTRA]].

*Despite the authors' claim that [[PTRA]] offered "little benefit" in comparison to [[pharmacological treatments]], [[patients]] in the [[PTRA]] community were less likely over 12 months of follow-up to experience regression in their [[blood pressure]] regulation or [[renal artery occlusion]].

===Renal Artery Stenting===

*[[Renal artery stenting]] is considered to be safe<ref name="pmid9715856">{{cite journal |vauthors=Dorros G, Jaff M, Mathiak L, Dorros II, Lowe A, Murphy K, He T |title=Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis |journal=Circulation |volume=98 |issue=7 |pages=642–7 |date=August 1998 |pmid=9715856 |doi=10.1161/01.cir.98.7.642 |url=}}</ref> and one of the effective<ref name="pmid9017938">{{cite journal |vauthors=Blum U, Krumme B, Flügel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M |title=Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty |journal=N Engl J Med |volume=336 |issue=7 |pages=459–65 |date=February 1997 |pmid=9017938 |doi=10.1056/NEJM199702133360702 |url=}}</ref> procedures involved in the management of [[renal artery stenosis]].
*In a meta-analysis conducted in the past showed promising results with [[stent placement]] along with higher [[success rates]] (98% vs 77%) and less risk of [[restenosis]] (17% vs 26%)<ref name="pmid10887230">{{cite journal |vauthors=Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In 't Veld AJ |title=Stent placement for renal arterial stenosis: where do we stand? A meta-analysis |journal=Radiology |volume=216 |issue=1 |pages=78–85 |date=July 2000 |pmid=10887230 |doi=10.1148/radiology.216.1.r00jl0778 |url=}}</ref> as compared to what with [[PTRA]].
*A randomized analysis revealed the effectiveness of [[renal stenting]] versus [[PTRA]] for rapid procedural success (88% versus 57%) and lower rates of [[restenosis]] (14 percent vs 48 percent, respectively) 70.
*In patients with [[ARAS]] and progressive [[renal insufficiency]], other studies have indicated recovery or stability of [[renal function]] after unilateral or [[bilateral renal stenting]]..71,72
*After therapy with at least 2 [[antihypertensive drugs]], in patients with [[ARAS]] and [[hypertension]] (blood pressure >140/90 mm Hg), renal stenting resulted in a 20 mm Hg decrease in [[systolic blood pressure]] and 1 less [[antihypertensive drug]].73
*The [[ASTRAL]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> ( [[Angioplasty]] and [[Stenting]] for [[Renal Artery Lesions]]) and the [[STAR]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> (Atherosclerotic Renal Artery Stenosis and Impaired Renal Function) trials, CORAL<ref name="pmid16824832">{{cite journal |vauthors=Cooper CJ, Murphy TP, Matsumoto A, Steffes M, Cohen DJ, Jaff M, Kuntz R, Jamerson K, Reid D, Rosenfield K, Rundback J, D'Agostino R, Henrich W, Dworkin L |title=Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: rationale and design of the CORAL trial |journal=Am Heart J |volume=152 |issue=1 |pages=59–66 |date=July 2006 |pmid=16824832 |doi=10.1016/j.ahj.2005.09.011 |url=}}</ref> (Cardiovascular Outcomes in [[Renal]] [[Atherosclerotic]] Lesions) are the major trials conducted for analyzing the importance of [[renal artery stenting]] in the management of [[renal artery stenosis]].

===Additional Interventional Procedures===
*While [[brachytherapy]] and cutting [[balloon atherotomy]]<ref name="pmid15152154">{{cite journal |vauthors=Jahraus CD, Meigooni AS |title=Vascular brachytherapy: a new approach to renal artery in-stent restenosis |journal=J Invasive Cardiol |volume=16 |issue=4 |pages=224–7; quiz (page following) |date=April 2004 |pmid=15152154 |doi= |url=}}</ref><ref name="pmid15553312">{{cite journal |vauthors=Otah KE, Alhaddad IA |title=Intravascular ultrasound-guided cutting [[balloon angioplasty]] for [[renal artery]] [[stent]] [[restenosis]] |journal=Clin Cardiol |volume=27 |issue=10 |pages=581–3 |date=October 2004 |pmid=15553312 |pmc=6654343 |doi=10.1002/clc.4960271012 |url=}}</ref> for [[renal artery]] in-stent restenosis have been used successfully, long-term findings are uncertain.

*[[Coronary]] [[drug-eluting stent]] usage<ref name="pmid15619320">{{cite journal |vauthors=Granillo GA, van Dijk LC, McFadden EP, Serruys PW |title=Percutaneous radial intervention for complex bilateral renal artery stenosis using paclitaxel eluting stents |journal=Catheter Cardiovasc Interv |volume=64 |issue=1 |pages=23–7 |date=January 2005 |pmid=15619320 |doi=10.1002/ccd.20240 |url=}}</ref> has also been identified for narrow [[renal arteries]], but there is a shortage of well-designed trials to evaluate the adequate eluting drug dosage for this vessel

*The major [[drug-eluting stent]] is just 3.5 mm in diameter, which is an inappropriate dimension for stenting of a [[renal artery]] (with a normal diameter of 4-7 mm). In order to trap atherosclerotic debris and avoid [[distal embolization]] during [[renal stenting]], 80 distal embolic safety systems have also been used, which may help maintain [[renal function]].

===Surgery===
*[[Surgical revascularization]]<ref name="pmid6700670">{{cite journal |vauthors=White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML |title=Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? |journal=N Engl J Med |volume=310 |issue=13 |pages=819–24 |date=March 1984 |pmid=6700670 |doi=10.1056/NEJM198403293101304 |url=}}</ref> is one of the effective modalities involved in the management of [[Renal artery stenosis]]. But the [[morbidity]] and [[mortality]] are higher with [[surgery]] as compared to [[stenting]].

*In one of the few trials comparing ostial [[ARAS]] [[surgical]] [[revascularization]] with [[percutaneous revascularization]], Balzer et al81 observed no substantial difference in long-term [[morbidity]] or [[mortality]] and no significant difference in [[blood pressure]] reduction.

*These findings show that [[surgical revascularization]] of ostial [[ARAS]] could be at least equal to [[PTRA]].

==References==

Renal artery stenosis medical therapy

2020-12-12T20:22:08Z

Shivam Singla: /* Additional Interventional Procedures */

__NOTOC__

{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

{{Renal artery stenosis}}

==Overview==
Patients with [[Renal artery stenosis]] require the widespread use of intensive [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in [[renal]] function after using the [[ACE inhibitors]] and [[ARB]], but it is neither a sensitive nor specific finding. Aggressive [[statin]] use, optimal [[glycemic]] regulation, and therapy for [[smoking]] abstinence are of vital significance. Other modalities used are [[renal artery]] [[revascularization]], [[Percutaneous transluminal renal angioplasty]], [[Renal artery stenting]], [[brachytherapy]] and cutting [[balloon atherotomy]], and [[surgery]] in complicated and nonresponding cases. Although [[morbidity]] and [[mortality]] are higher associated with [[surgery]] as compared to stenting.

==Treatment==

===Medical Therapy===
Patients with [[Renal artery stenosis]] require the widespread use of [[intensive]] [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in the [[renal function]] after using the [[ACE inhibitors]] and [[ARB]], but it is neither sensitive nor specific<ref name="pmid6337327">{{cite journal |vauthors=Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ |title=Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney |journal=N Engl J Med |volume=308 |issue=7 |pages=373–6 |date=February 1983 |pmid=6337327 |doi=10.1056/NEJM198302173080706 |url=}}</ref>. Aggressive [[statin]] use, optimal [[glycemic regulation]], and therapy for [[smoking]] abstinence are of vital significance.

Aggressive use of [[statins]], optimal [[glycemic control]], and [[smoking]] cessation counseling is of paramount importance. The results of various medical regimens on the treatment of [[ARAS]]-related [[hypertension]] were not analyzed in a [[randomized clinical trial]] because such [[patients]] frequently have [[refractory]] [[hypertension]] and need multiple [[antihypertensive]] [[medicines]]. [[Medical therapy]] is preferred for [[revascularization]] in [[patients]] with [[ARAS]] and progressive [[renal disease]] (i.e. chronic renal dysfunction, proteinuria[>1 g/d]), diffuse [[intrarenal vascular disease]], and [[renal atrophy]]<ref name="pmid15580159">{{cite journal |vauthors=Bokhari SW, Faxon DP |title=Current advances in the diagnosis and treatment of renal artery stenosis |journal=Rev Cardiovasc Med |volume=5 |issue=4 |pages=204–15 |date=2004 |pmid=15580159 |doi= |url=}}</ref>.

===Renal Artery Revascularization===
It is less obvious and much more contentious whether [[patients]] with [[ARAS]] and [[hypertension]] would undergo [[surgical revascularization]]. According to studies [[patients]] with extreme [[ostial]] [[renal artery stenosis]] who have been successfully [[revascularized]] [[percutaneously]] do not necessarily have therapeutic benefits.

The ACC/AHA description of [[RAS]] is as follows:

(1) visually approximate [[stenosis]] of 50 percent to 70 percent diameter with a translational peak gradient of at least 20 mm Hg or a mean gradient of at least 10 mm Hg

(2) [[angiographic stenosis]] of at least 70 percent diameter

(3) greater than 70% stenosis according to the measurement by [[intravascular ultrasounds]]<ref name="pmid8178389">{{cite journal |vauthors=Olin JW |title=Role of duplex ultrasonography in screening for significant renal artery disease |journal=Urol Clin North Am |volume=21 |issue=2 |pages=215–26 |date=May 1994 |pmid=8178389 |doi= |url=}}</ref>.

Present ACC/AHA recommendations do not, however, include these steps and prescribe [[revascularization]] of [[ARAS]] only when it is associated with certain [[medical conditions]] mentioned as follows:

1) Asymptomatic [[stenosis]]: [[Percutaneous revascularization]] can be considered for the treatment of:

*An asymptomatic bilateral

*Solitary viable [[kidney]] with [[thermodynamically]] significant [[ARAS]] (class Jib, degree of proof II.OF.I C),.

*The efficacy of [[percutaneous]] or asymptomatic unilateral hemodynamically significant [[ARAS]] in a viable kidney is not well known and clinically unrecognized (class 11b, LOE C)

2) [[Hypertension]]

*[[Percutaneous revascularization]] is used for patients with
*Hemodynamically significant [[renal artery stenosis]] along with accelerated [[hypertension]]
*[[Malignant hypertension]]
*[[Resistant hypertension]]
*In cases with [[hypertension]] and associated [[unilateral small kidney]].

3) Preservation of [[renal function]]

*[[Percutaneous revascularization]] is helpful in patients with [[ARAS]] + [[Chronic progressive kidney disease]] with [[bilateral renal artery stenosis]] or solitary functioning [[kidney]]. (Class IIa, LOE B)

*Also considered significant in [[patients]] with [[RAS]] and [[chronic renal insufficiency]] with [[unilateral renal artery stenosis]]. (Class IIb, LOE C)

4) Effects of [[renal artery stenosis]] on [[Congestive heart failure]] and [[unstable angina]]: [[Percutaneous revascularization]] is considered in [[patients]] with

*[[RAS]] + Recurrent [[congestive heart failure]] or sudden unexplained [[pulmonary edema]]. (Class I, LOE B)
*[[Patients]] with hemodynamically significant [[RAS]] along with [[unstable angina]] (Class IIa, LOE B)

 

===Percutaneous Transluminal Renal Angioplasty===
*Dutch [[Renal Artery Stenosis]] Intervention Cooperative (DRASTIC)<ref name="pmid10749962">{{cite journal |vauthors=van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in 't Veld AJ, Schalekamp MA |title=The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group |journal=N Engl J Med |volume=342 |issue=14 |pages=1007–14 |date=April 2000 |pmid=10749962 |doi=10.1056/NEJM200004063421403 |url=}}</ref> did a study to compare the effects of [[drug treatment]] and [[PTRA]].

*Despite the authors' claim that [[PTRA]] offered "little benefit" in comparison to [[pharmacological treatments]], [[patients]] in the [[PTRA]] community were less likely over 12 months of follow-up to experience regression in their [[blood pressure]] regulation or [[renal artery occlusion]].

===Renal Artery Stenting===

*[[Renal artery stenting]] is considered to be safe<ref name="pmid9715856">{{cite journal |vauthors=Dorros G, Jaff M, Mathiak L, Dorros II, Lowe A, Murphy K, He T |title=Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis |journal=Circulation |volume=98 |issue=7 |pages=642–7 |date=August 1998 |pmid=9715856 |doi=10.1161/01.cir.98.7.642 |url=}}</ref> and one of the effective<ref name="pmid9017938">{{cite journal |vauthors=Blum U, Krumme B, Flügel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M |title=Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty |journal=N Engl J Med |volume=336 |issue=7 |pages=459–65 |date=February 1997 |pmid=9017938 |doi=10.1056/NEJM199702133360702 |url=}}</ref> procedures involved in the management of [[renal artery stenosis]].
*In a meta-analysis conducted in the past showed promising results with [[stent placement]] along with higher [[success rates]] (98% vs 77%) and less risk of [[restenosis]] (17% vs 26%)<ref name="pmid10887230">{{cite journal |vauthors=Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In 't Veld AJ |title=Stent placement for renal arterial stenosis: where do we stand? A meta-analysis |journal=Radiology |volume=216 |issue=1 |pages=78–85 |date=July 2000 |pmid=10887230 |doi=10.1148/radiology.216.1.r00jl0778 |url=}}</ref> as compared to what with [[PTRA]].
*A randomized analysis revealed the effectiveness of [[renal stenting]] versus [[PTRA]] for rapid procedural success (88% versus 57%) and lower rates of [[restenosis]] (14 percent vs 48 percent, respectively) 70.
*In patients with [[ARAS]] and progressive [[renal insufficiency]], other studies have indicated recovery or stability of [[renal function]] after unilateral or [[bilateral renal stenting]]..71,72
*After therapy with at least 2 [[antihypertensive drugs]], in patients with [[ARAS]] and [[hypertension]] (blood pressure >140/90 mm Hg), renal stenting resulted in a 20 mm Hg decrease in [[systolic blood pressure]] and 1 less [[antihypertensive drug]].73
*The [[ASTRAL]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> ( [[Angioplasty]] and [[Stenting]] for [[Renal Artery Lesions]]) and the [[STAR]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> (Atherosclerotic Renal Artery Stenosis and Impaired Renal Function) trials, CORAL<ref name="pmid16824832">{{cite journal |vauthors=Cooper CJ, Murphy TP, Matsumoto A, Steffes M, Cohen DJ, Jaff M, Kuntz R, Jamerson K, Reid D, Rosenfield K, Rundback J, D'Agostino R, Henrich W, Dworkin L |title=Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: rationale and design of the CORAL trial |journal=Am Heart J |volume=152 |issue=1 |pages=59–66 |date=July 2006 |pmid=16824832 |doi=10.1016/j.ahj.2005.09.011 |url=}}</ref> (Cardiovascular Outcomes in [[Renal]] [[Atherosclerotic]] Lesions) are the major trials conducted for analyzing the importance of [[renal artery stenting]] in the management of [[renal artery stenosis]].

===Additional Interventional Procedures===
*While [[brachytherapy]] and cutting [[balloon atherotomy]]<ref name="pmid15152154">{{cite journal |vauthors=Jahraus CD, Meigooni AS |title=Vascular brachytherapy: a new approach to renal artery in-stent restenosis |journal=J Invasive Cardiol |volume=16 |issue=4 |pages=224–7; quiz (page following) |date=April 2004 |pmid=15152154 |doi= |url=}}</ref><ref name="pmid15553312">{{cite journal |vauthors=Otah KE, Alhaddad IA |title=Intravascular ultrasound-guided cutting [[balloon angioplasty]] for [[renal artery]] [[stent]] [[restenosis]] |journal=Clin Cardiol |volume=27 |issue=10 |pages=581–3 |date=October 2004 |pmid=15553312 |pmc=6654343 |doi=10.1002/clc.4960271012 |url=}}</ref> for [[renal artery]] in-stent restenosis have been used successfully, long-term findings are uncertain.

*[[Coronary]] [[drug-eluting stent]] usage<ref name="pmid15619320">{{cite journal |vauthors=Granillo GA, van Dijk LC, McFadden EP, Serruys PW |title=Percutaneous radial intervention for complex bilateral renal artery stenosis using paclitaxel eluting stents |journal=Catheter Cardiovasc Interv |volume=64 |issue=1 |pages=23–7 |date=January 2005 |pmid=15619320 |doi=10.1002/ccd.20240 |url=}}</ref> has also been identified for narrow [[renal arteries]], but there is a shortage of well-designed trials to evaluate the adequate eluting drug dosage for this vessel

*The major [[drug-eluting stent]] is just 3.5 mm in diameter, which is an inappropriate dimension for stenting of a [[renal artery]] (with a normal diameter of 4-7 mm). In order to trap atherosclerotic debris and avoid [[distal embolization]] during [[renal stenting]], 80 distal embolic safety systems have also been used, which may help maintain [[renal function]].

===Surgery===
*Surgical revascularization<ref name="pmid6700670">{{cite journal |vauthors=White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML |title=Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? |journal=N Engl J Med |volume=310 |issue=13 |pages=819–24 |date=March 1984 |pmid=6700670 |doi=10.1056/NEJM198403293101304 |url=}}</ref> is one of the effective modalities involved in the management of Renal artery stenosis. But the morbidity and mortality are higher with surgery as compared to stenting.

*In one of the few trials comparing ostial ARAS surgical revascularization with percutaneous revascularization, Balzer et al81 observed no substantial difference in long-term morbidity or mortality and no significant difference in blood pressure reduction.

*These findings show that surgical revascularization of ostial ARAS could be at least equal to PTRA. 

==References==

Renal artery stenosis medical therapy

2020-12-12T20:18:31Z

Shivam Singla: /* Renal Artery Stenting */

__NOTOC__

{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

{{Renal artery stenosis}}

==Overview==
Patients with [[Renal artery stenosis]] require the widespread use of intensive [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in [[renal]] function after using the [[ACE inhibitors]] and [[ARB]], but it is neither a sensitive nor specific finding. Aggressive [[statin]] use, optimal [[glycemic]] regulation, and therapy for [[smoking]] abstinence are of vital significance. Other modalities used are [[renal artery]] [[revascularization]], [[Percutaneous transluminal renal angioplasty]], [[Renal artery stenting]], [[brachytherapy]] and cutting [[balloon atherotomy]], and [[surgery]] in complicated and nonresponding cases. Although [[morbidity]] and [[mortality]] are higher associated with [[surgery]] as compared to stenting.

==Treatment==

===Medical Therapy===
Patients with [[Renal artery stenosis]] require the widespread use of [[intensive]] [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in the [[renal function]] after using the [[ACE inhibitors]] and [[ARB]], but it is neither sensitive nor specific<ref name="pmid6337327">{{cite journal |vauthors=Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ |title=Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney |journal=N Engl J Med |volume=308 |issue=7 |pages=373–6 |date=February 1983 |pmid=6337327 |doi=10.1056/NEJM198302173080706 |url=}}</ref>. Aggressive [[statin]] use, optimal [[glycemic regulation]], and therapy for [[smoking]] abstinence are of vital significance.

Aggressive use of [[statins]], optimal [[glycemic control]], and [[smoking]] cessation counseling is of paramount importance. The results of various medical regimens on the treatment of [[ARAS]]-related [[hypertension]] were not analyzed in a [[randomized clinical trial]] because such [[patients]] frequently have [[refractory]] [[hypertension]] and need multiple [[antihypertensive]] [[medicines]]. [[Medical therapy]] is preferred for [[revascularization]] in [[patients]] with [[ARAS]] and progressive [[renal disease]] (i.e. chronic renal dysfunction, proteinuria[>1 g/d]), diffuse [[intrarenal vascular disease]], and [[renal atrophy]]<ref name="pmid15580159">{{cite journal |vauthors=Bokhari SW, Faxon DP |title=Current advances in the diagnosis and treatment of renal artery stenosis |journal=Rev Cardiovasc Med |volume=5 |issue=4 |pages=204–15 |date=2004 |pmid=15580159 |doi= |url=}}</ref>.

===Renal Artery Revascularization===
It is less obvious and much more contentious whether [[patients]] with [[ARAS]] and [[hypertension]] would undergo [[surgical revascularization]]. According to studies [[patients]] with extreme [[ostial]] [[renal artery stenosis]] who have been successfully [[revascularized]] [[percutaneously]] do not necessarily have therapeutic benefits.

The ACC/AHA description of [[RAS]] is as follows:

(1) visually approximate [[stenosis]] of 50 percent to 70 percent diameter with a translational peak gradient of at least 20 mm Hg or a mean gradient of at least 10 mm Hg

(2) [[angiographic stenosis]] of at least 70 percent diameter

(3) greater than 70% stenosis according to the measurement by [[intravascular ultrasounds]]<ref name="pmid8178389">{{cite journal |vauthors=Olin JW |title=Role of duplex ultrasonography in screening for significant renal artery disease |journal=Urol Clin North Am |volume=21 |issue=2 |pages=215–26 |date=May 1994 |pmid=8178389 |doi= |url=}}</ref>.

Present ACC/AHA recommendations do not, however, include these steps and prescribe [[revascularization]] of [[ARAS]] only when it is associated with certain [[medical conditions]] mentioned as follows:

1) Asymptomatic [[stenosis]]: [[Percutaneous revascularization]] can be considered for the treatment of:

*An asymptomatic bilateral

*Solitary viable [[kidney]] with [[thermodynamically]] significant [[ARAS]] (class Jib, degree of proof II.OF.I C),.

*The efficacy of [[percutaneous]] or asymptomatic unilateral hemodynamically significant [[ARAS]] in a viable kidney is not well known and clinically unrecognized (class 11b, LOE C)

2) [[Hypertension]]

*[[Percutaneous revascularization]] is used for patients with
*Hemodynamically significant [[renal artery stenosis]] along with accelerated [[hypertension]]
*[[Malignant hypertension]]
*[[Resistant hypertension]]
*In cases with [[hypertension]] and associated [[unilateral small kidney]].

3) Preservation of [[renal function]]

*[[Percutaneous revascularization]] is helpful in patients with [[ARAS]] + [[Chronic progressive kidney disease]] with [[bilateral renal artery stenosis]] or solitary functioning [[kidney]]. (Class IIa, LOE B)

*Also considered significant in [[patients]] with [[RAS]] and [[chronic renal insufficiency]] with [[unilateral renal artery stenosis]]. (Class IIb, LOE C)

4) Effects of [[renal artery stenosis]] on [[Congestive heart failure]] and [[unstable angina]]: [[Percutaneous revascularization]] is considered in [[patients]] with

*[[RAS]] + Recurrent [[congestive heart failure]] or sudden unexplained [[pulmonary edema]]. (Class I, LOE B)
*[[Patients]] with hemodynamically significant [[RAS]] along with [[unstable angina]] (Class IIa, LOE B)

 

===Percutaneous Transluminal Renal Angioplasty===
*Dutch [[Renal Artery Stenosis]] Intervention Cooperative (DRASTIC)<ref name="pmid10749962">{{cite journal |vauthors=van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in 't Veld AJ, Schalekamp MA |title=The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group |journal=N Engl J Med |volume=342 |issue=14 |pages=1007–14 |date=April 2000 |pmid=10749962 |doi=10.1056/NEJM200004063421403 |url=}}</ref> did a study to compare the effects of [[drug treatment]] and [[PTRA]].

*Despite the authors' claim that [[PTRA]] offered "little benefit" in comparison to [[pharmacological treatments]], [[patients]] in the [[PTRA]] community were less likely over 12 months of follow-up to experience regression in their [[blood pressure]] regulation or [[renal artery occlusion]].

===Renal Artery Stenting===

*[[Renal artery stenting]] is considered to be safe<ref name="pmid9715856">{{cite journal |vauthors=Dorros G, Jaff M, Mathiak L, Dorros II, Lowe A, Murphy K, He T |title=Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis |journal=Circulation |volume=98 |issue=7 |pages=642–7 |date=August 1998 |pmid=9715856 |doi=10.1161/01.cir.98.7.642 |url=}}</ref> and one of the effective<ref name="pmid9017938">{{cite journal |vauthors=Blum U, Krumme B, Flügel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M |title=Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty |journal=N Engl J Med |volume=336 |issue=7 |pages=459–65 |date=February 1997 |pmid=9017938 |doi=10.1056/NEJM199702133360702 |url=}}</ref> procedures involved in the management of [[renal artery stenosis]].
*In a meta-analysis conducted in the past showed promising results with [[stent placement]] along with higher [[success rates]] (98% vs 77%) and less risk of [[restenosis]] (17% vs 26%)<ref name="pmid10887230">{{cite journal |vauthors=Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In 't Veld AJ |title=Stent placement for renal arterial stenosis: where do we stand? A meta-analysis |journal=Radiology |volume=216 |issue=1 |pages=78–85 |date=July 2000 |pmid=10887230 |doi=10.1148/radiology.216.1.r00jl0778 |url=}}</ref> as compared to what with [[PTRA]].
*A randomized analysis revealed the effectiveness of [[renal stenting]] versus [[PTRA]] for rapid procedural success (88% versus 57%) and lower rates of [[restenosis]] (14 percent vs 48 percent, respectively) 70.
*In patients with [[ARAS]] and progressive [[renal insufficiency]], other studies have indicated recovery or stability of [[renal function]] after unilateral or [[bilateral renal stenting]]..71,72
*After therapy with at least 2 [[antihypertensive drugs]], in patients with [[ARAS]] and [[hypertension]] (blood pressure >140/90 mm Hg), renal stenting resulted in a 20 mm Hg decrease in [[systolic blood pressure]] and 1 less [[antihypertensive drug]].73
*The [[ASTRAL]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> ( [[Angioplasty]] and [[Stenting]] for [[Renal Artery Lesions]]) and the [[STAR]]<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> (Atherosclerotic Renal Artery Stenosis and Impaired Renal Function) trials, CORAL<ref name="pmid16824832">{{cite journal |vauthors=Cooper CJ, Murphy TP, Matsumoto A, Steffes M, Cohen DJ, Jaff M, Kuntz R, Jamerson K, Reid D, Rosenfield K, Rundback J, D'Agostino R, Henrich W, Dworkin L |title=Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: rationale and design of the CORAL trial |journal=Am Heart J |volume=152 |issue=1 |pages=59–66 |date=July 2006 |pmid=16824832 |doi=10.1016/j.ahj.2005.09.011 |url=}}</ref> (Cardiovascular Outcomes in [[Renal]] [[Atherosclerotic]] Lesions) are the major trials conducted for analyzing the importance of [[renal artery stenting]] in the management of [[renal artery stenosis]].

===Additional Interventional Procedures===
*While brachytherapy and cutting balloon atherotomy<ref name="pmid15152154">{{cite journal |vauthors=Jahraus CD, Meigooni AS |title=Vascular brachytherapy: a new approach to renal artery in-stent restenosis |journal=J Invasive Cardiol |volume=16 |issue=4 |pages=224–7; quiz (page following) |date=April 2004 |pmid=15152154 |doi= |url=}}</ref><ref name="pmid15553312">{{cite journal |vauthors=Otah KE, Alhaddad IA |title=Intravascular ultrasound-guided cutting balloon angioplasty for renal artery stent restenosis |journal=Clin Cardiol |volume=27 |issue=10 |pages=581–3 |date=October 2004 |pmid=15553312 |pmc=6654343 |doi=10.1002/clc.4960271012 |url=}}</ref> for renal artery in-stent restenosis have been used successfully, long-term findings are uncertain.

*Coronary drug-eluting stent usage<ref name="pmid15619320">{{cite journal |vauthors=Granillo GA, van Dijk LC, McFadden EP, Serruys PW |title=Percutaneous radial intervention for complex bilateral renal artery stenosis using paclitaxel eluting stents |journal=Catheter Cardiovasc Interv |volume=64 |issue=1 |pages=23–7 |date=January 2005 |pmid=15619320 |doi=10.1002/ccd.20240 |url=}}</ref> has also been identified for narrow renal arteries, but there is a shortage of well-designed trials to evaluate the adequate eluting drug dosage for this vessel

*The major drug-eluting stent is just 3.5 mm in diameter, which is an inappropriate dimension for stenting of a renal artery (with a normal diameter of 4-7 mm). In order to trap atherosclerotic debris and avoid distal embolization during renal stenting, 80 distal embolic safety systems have also been used, which may help maintain renal function.

===Surgery===
*Surgical revascularization<ref name="pmid6700670">{{cite journal |vauthors=White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML |title=Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? |journal=N Engl J Med |volume=310 |issue=13 |pages=819–24 |date=March 1984 |pmid=6700670 |doi=10.1056/NEJM198403293101304 |url=}}</ref> is one of the effective modalities involved in the management of Renal artery stenosis. But the morbidity and mortality are higher with surgery as compared to stenting.

*In one of the few trials comparing ostial ARAS surgical revascularization with percutaneous revascularization, Balzer et al81 observed no substantial difference in long-term morbidity or mortality and no significant difference in blood pressure reduction.

*These findings show that surgical revascularization of ostial ARAS could be at least equal to PTRA. 

==References==

Renal artery stenosis medical therapy

2020-12-12T20:14:51Z

Shivam Singla: /* Percutaneous Transluminal Renal Angioplasty */

__NOTOC__

{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

{{Renal artery stenosis}}

==Overview==
Patients with [[Renal artery stenosis]] require the widespread use of intensive [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in [[renal]] function after using the [[ACE inhibitors]] and [[ARB]], but it is neither a sensitive nor specific finding. Aggressive [[statin]] use, optimal [[glycemic]] regulation, and therapy for [[smoking]] abstinence are of vital significance. Other modalities used are [[renal artery]] [[revascularization]], [[Percutaneous transluminal renal angioplasty]], [[Renal artery stenting]], [[brachytherapy]] and cutting [[balloon atherotomy]], and [[surgery]] in complicated and nonresponding cases. Although [[morbidity]] and [[mortality]] are higher associated with [[surgery]] as compared to stenting.

==Treatment==

===Medical Therapy===
Patients with [[Renal artery stenosis]] require the widespread use of [[intensive]] [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in the [[renal function]] after using the [[ACE inhibitors]] and [[ARB]], but it is neither sensitive nor specific<ref name="pmid6337327">{{cite journal |vauthors=Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ |title=Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney |journal=N Engl J Med |volume=308 |issue=7 |pages=373–6 |date=February 1983 |pmid=6337327 |doi=10.1056/NEJM198302173080706 |url=}}</ref>. Aggressive [[statin]] use, optimal [[glycemic regulation]], and therapy for [[smoking]] abstinence are of vital significance.

Aggressive use of [[statins]], optimal [[glycemic control]], and [[smoking]] cessation counseling is of paramount importance. The results of various medical regimens on the treatment of [[ARAS]]-related [[hypertension]] were not analyzed in a [[randomized clinical trial]] because such [[patients]] frequently have [[refractory]] [[hypertension]] and need multiple [[antihypertensive]] [[medicines]]. [[Medical therapy]] is preferred for [[revascularization]] in [[patients]] with [[ARAS]] and progressive [[renal disease]] (i.e. chronic renal dysfunction, proteinuria[>1 g/d]), diffuse [[intrarenal vascular disease]], and [[renal atrophy]]<ref name="pmid15580159">{{cite journal |vauthors=Bokhari SW, Faxon DP |title=Current advances in the diagnosis and treatment of renal artery stenosis |journal=Rev Cardiovasc Med |volume=5 |issue=4 |pages=204–15 |date=2004 |pmid=15580159 |doi= |url=}}</ref>.

===Renal Artery Revascularization===
It is less obvious and much more contentious whether [[patients]] with [[ARAS]] and [[hypertension]] would undergo [[surgical revascularization]]. According to studies [[patients]] with extreme [[ostial]] [[renal artery stenosis]] who have been successfully [[revascularized]] [[percutaneously]] do not necessarily have therapeutic benefits.

The ACC/AHA description of [[RAS]] is as follows:

(1) visually approximate [[stenosis]] of 50 percent to 70 percent diameter with a translational peak gradient of at least 20 mm Hg or a mean gradient of at least 10 mm Hg

(2) [[angiographic stenosis]] of at least 70 percent diameter

(3) greater than 70% stenosis according to the measurement by [[intravascular ultrasounds]]<ref name="pmid8178389">{{cite journal |vauthors=Olin JW |title=Role of duplex ultrasonography in screening for significant renal artery disease |journal=Urol Clin North Am |volume=21 |issue=2 |pages=215–26 |date=May 1994 |pmid=8178389 |doi= |url=}}</ref>.

Present ACC/AHA recommendations do not, however, include these steps and prescribe [[revascularization]] of [[ARAS]] only when it is associated with certain [[medical conditions]] mentioned as follows:

1) Asymptomatic [[stenosis]]: [[Percutaneous revascularization]] can be considered for the treatment of:

*An asymptomatic bilateral

*Solitary viable [[kidney]] with [[thermodynamically]] significant [[ARAS]] (class Jib, degree of proof II.OF.I C),.

*The efficacy of [[percutaneous]] or asymptomatic unilateral hemodynamically significant [[ARAS]] in a viable kidney is not well known and clinically unrecognized (class 11b, LOE C)

2) [[Hypertension]]

*[[Percutaneous revascularization]] is used for patients with
*Hemodynamically significant [[renal artery stenosis]] along with accelerated [[hypertension]]
*[[Malignant hypertension]]
*[[Resistant hypertension]]
*In cases with [[hypertension]] and associated [[unilateral small kidney]].

3) Preservation of [[renal function]]

*[[Percutaneous revascularization]] is helpful in patients with [[ARAS]] + [[Chronic progressive kidney disease]] with [[bilateral renal artery stenosis]] or solitary functioning [[kidney]]. (Class IIa, LOE B)

*Also considered significant in [[patients]] with [[RAS]] and [[chronic renal insufficiency]] with [[unilateral renal artery stenosis]]. (Class IIb, LOE C)

4) Effects of [[renal artery stenosis]] on [[Congestive heart failure]] and [[unstable angina]]: [[Percutaneous revascularization]] is considered in [[patients]] with

*[[RAS]] + Recurrent [[congestive heart failure]] or sudden unexplained [[pulmonary edema]]. (Class I, LOE B)
*[[Patients]] with hemodynamically significant [[RAS]] along with [[unstable angina]] (Class IIa, LOE B)

 

===Percutaneous Transluminal Renal Angioplasty===
*Dutch [[Renal Artery Stenosis]] Intervention Cooperative (DRASTIC)<ref name="pmid10749962">{{cite journal |vauthors=van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in 't Veld AJ, Schalekamp MA |title=The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group |journal=N Engl J Med |volume=342 |issue=14 |pages=1007–14 |date=April 2000 |pmid=10749962 |doi=10.1056/NEJM200004063421403 |url=}}</ref> did a study to compare the effects of [[drug treatment]] and [[PTRA]].

*Despite the authors' claim that [[PTRA]] offered "little benefit" in comparison to [[pharmacological treatments]], [[patients]] in the [[PTRA]] community were less likely over 12 months of follow-up to experience regression in their [[blood pressure]] regulation or [[renal artery occlusion]].

===Renal Artery Stenting===

*Renal artery stenting is considered to be safe<ref name="pmid9715856">{{cite journal |vauthors=Dorros G, Jaff M, Mathiak L, Dorros II, Lowe A, Murphy K, He T |title=Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis |journal=Circulation |volume=98 |issue=7 |pages=642–7 |date=August 1998 |pmid=9715856 |doi=10.1161/01.cir.98.7.642 |url=}}</ref> and one of the effective<ref name="pmid9017938">{{cite journal |vauthors=Blum U, Krumme B, Flügel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M |title=Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty |journal=N Engl J Med |volume=336 |issue=7 |pages=459–65 |date=February 1997 |pmid=9017938 |doi=10.1056/NEJM199702133360702 |url=}}</ref> procedures involved in the management of renal artery stenosis.
*In a meta-analysis conducted in the past showed promising results with stent placement along with higher success rates (98% vs 77%) and less risk of restenosis (17% vs 26%)<ref name="pmid10887230">{{cite journal |vauthors=Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In 't Veld AJ |title=Stent placement for renal arterial stenosis: where do we stand? A meta-analysis |journal=Radiology |volume=216 |issue=1 |pages=78–85 |date=July 2000 |pmid=10887230 |doi=10.1148/radiology.216.1.r00jl0778 |url=}}</ref> as compared to what with PTRA.
*A randomized analysis revealed the effectiveness of renal stenting versus PTRA for rapid procedural success (88% versus 57%) and lower rates of restenosis (14 percent vs 48 percent, respectively) 70.
*In patients with ARAS and progressive renal insufficiency, other studies have indicated recovery or stability of renal function after unilateral or bilateral renal stenting..71,72
*After therapy with at least 2 antihypertensive drugs, in patients with ARAS and hypertension (blood pressure >140/90 mm Hg), renal stenting resulted in a 20 mm Hg decrease in systolic blood pressure and 1 less antihypertensive drug.73
*The ASTRAL<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> ( Angioplasty and Stenting for Renal Artery Lesions) and the STAR<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> (Atherosclerotic Renal Artery Stenosis and Impaired Renal Function) trials, CORAL<ref name="pmid16824832">{{cite journal |vauthors=Cooper CJ, Murphy TP, Matsumoto A, Steffes M, Cohen DJ, Jaff M, Kuntz R, Jamerson K, Reid D, Rosenfield K, Rundback J, D'Agostino R, Henrich W, Dworkin L |title=Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: rationale and design of the CORAL trial |journal=Am Heart J |volume=152 |issue=1 |pages=59–66 |date=July 2006 |pmid=16824832 |doi=10.1016/j.ahj.2005.09.011 |url=}}</ref> (Cardiovascular Outcomes in Renal Atherosclerotic Lesions) are the major trials conducted for analyzing the importance of renal artery stenting in the management of renal artery stenosis.

===Additional Interventional Procedures===
*While brachytherapy and cutting balloon atherotomy<ref name="pmid15152154">{{cite journal |vauthors=Jahraus CD, Meigooni AS |title=Vascular brachytherapy: a new approach to renal artery in-stent restenosis |journal=J Invasive Cardiol |volume=16 |issue=4 |pages=224–7; quiz (page following) |date=April 2004 |pmid=15152154 |doi= |url=}}</ref><ref name="pmid15553312">{{cite journal |vauthors=Otah KE, Alhaddad IA |title=Intravascular ultrasound-guided cutting balloon angioplasty for renal artery stent restenosis |journal=Clin Cardiol |volume=27 |issue=10 |pages=581–3 |date=October 2004 |pmid=15553312 |pmc=6654343 |doi=10.1002/clc.4960271012 |url=}}</ref> for renal artery in-stent restenosis have been used successfully, long-term findings are uncertain.

*Coronary drug-eluting stent usage<ref name="pmid15619320">{{cite journal |vauthors=Granillo GA, van Dijk LC, McFadden EP, Serruys PW |title=Percutaneous radial intervention for complex bilateral renal artery stenosis using paclitaxel eluting stents |journal=Catheter Cardiovasc Interv |volume=64 |issue=1 |pages=23–7 |date=January 2005 |pmid=15619320 |doi=10.1002/ccd.20240 |url=}}</ref> has also been identified for narrow renal arteries, but there is a shortage of well-designed trials to evaluate the adequate eluting drug dosage for this vessel

*The major drug-eluting stent is just 3.5 mm in diameter, which is an inappropriate dimension for stenting of a renal artery (with a normal diameter of 4-7 mm). In order to trap atherosclerotic debris and avoid distal embolization during renal stenting, 80 distal embolic safety systems have also been used, which may help maintain renal function.

===Surgery===
*Surgical revascularization<ref name="pmid6700670">{{cite journal |vauthors=White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML |title=Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? |journal=N Engl J Med |volume=310 |issue=13 |pages=819–24 |date=March 1984 |pmid=6700670 |doi=10.1056/NEJM198403293101304 |url=}}</ref> is one of the effective modalities involved in the management of Renal artery stenosis. But the morbidity and mortality are higher with surgery as compared to stenting.

*In one of the few trials comparing ostial ARAS surgical revascularization with percutaneous revascularization, Balzer et al81 observed no substantial difference in long-term morbidity or mortality and no significant difference in blood pressure reduction.

*These findings show that surgical revascularization of ostial ARAS could be at least equal to PTRA. 

==References==

Renal artery stenosis medical therapy

2020-12-12T20:11:32Z

Shivam Singla: /* Renal Artery Revascularization */

__NOTOC__

{{CMG}}; '''Associate Editor-In-Chief:''' {{Shivam Singla}}

{{Renal artery stenosis}}

==Overview==
Patients with [[Renal artery stenosis]] require the widespread use of intensive [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in [[renal]] function after using the [[ACE inhibitors]] and [[ARB]], but it is neither a sensitive nor specific finding. Aggressive [[statin]] use, optimal [[glycemic]] regulation, and therapy for [[smoking]] abstinence are of vital significance. Other modalities used are [[renal artery]] [[revascularization]], [[Percutaneous transluminal renal angioplasty]], [[Renal artery stenting]], [[brachytherapy]] and cutting [[balloon atherotomy]], and [[surgery]] in complicated and nonresponding cases. Although [[morbidity]] and [[mortality]] are higher associated with [[surgery]] as compared to stenting.

==Treatment==

===Medical Therapy===
Patients with [[Renal artery stenosis]] require the widespread use of [[intensive]] [[medical therapy]]. The [[drugs]] responsible for the management of [[renal artery stenosis]] are [[ACE inhibitors]] or [[ARB's]]. These drugs inhibit the [[sympathetic]] and [[renin-angiotensin system]] resulting in controlling [[hypertension]]. In patients with bilateral [[renal artery stenosis]], there is an associated decrease in the [[renal function]] after using the [[ACE inhibitors]] and [[ARB]], but it is neither sensitive nor specific<ref name="pmid6337327">{{cite journal |vauthors=Hricik DE, Browning PJ, Kopelman R, Goorno WE, Madias NE, Dzau VJ |title=Captopril-induced functional renal insufficiency in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney |journal=N Engl J Med |volume=308 |issue=7 |pages=373–6 |date=February 1983 |pmid=6337327 |doi=10.1056/NEJM198302173080706 |url=}}</ref>. Aggressive [[statin]] use, optimal [[glycemic regulation]], and therapy for [[smoking]] abstinence are of vital significance.

Aggressive use of [[statins]], optimal [[glycemic control]], and [[smoking]] cessation counseling is of paramount importance. The results of various medical regimens on the treatment of [[ARAS]]-related [[hypertension]] were not analyzed in a [[randomized clinical trial]] because such [[patients]] frequently have [[refractory]] [[hypertension]] and need multiple [[antihypertensive]] [[medicines]]. [[Medical therapy]] is preferred for [[revascularization]] in [[patients]] with [[ARAS]] and progressive [[renal disease]] (i.e. chronic renal dysfunction, proteinuria[>1 g/d]), diffuse [[intrarenal vascular disease]], and [[renal atrophy]]<ref name="pmid15580159">{{cite journal |vauthors=Bokhari SW, Faxon DP |title=Current advances in the diagnosis and treatment of renal artery stenosis |journal=Rev Cardiovasc Med |volume=5 |issue=4 |pages=204–15 |date=2004 |pmid=15580159 |doi= |url=}}</ref>.

===Renal Artery Revascularization===
It is less obvious and much more contentious whether [[patients]] with [[ARAS]] and [[hypertension]] would undergo [[surgical revascularization]]. According to studies [[patients]] with extreme [[ostial]] [[renal artery stenosis]] who have been successfully [[revascularized]] [[percutaneously]] do not necessarily have therapeutic benefits.

The ACC/AHA description of [[RAS]] is as follows:

(1) visually approximate [[stenosis]] of 50 percent to 70 percent diameter with a translational peak gradient of at least 20 mm Hg or a mean gradient of at least 10 mm Hg

(2) [[angiographic stenosis]] of at least 70 percent diameter

(3) greater than 70% stenosis according to the measurement by [[intravascular ultrasounds]]<ref name="pmid8178389">{{cite journal |vauthors=Olin JW |title=Role of duplex ultrasonography in screening for significant renal artery disease |journal=Urol Clin North Am |volume=21 |issue=2 |pages=215–26 |date=May 1994 |pmid=8178389 |doi= |url=}}</ref>.

Present ACC/AHA recommendations do not, however, include these steps and prescribe [[revascularization]] of [[ARAS]] only when it is associated with certain [[medical conditions]] mentioned as follows:

1) Asymptomatic [[stenosis]]: [[Percutaneous revascularization]] can be considered for the treatment of:

*An asymptomatic bilateral

*Solitary viable [[kidney]] with [[thermodynamically]] significant [[ARAS]] (class Jib, degree of proof II.OF.I C),.

*The efficacy of [[percutaneous]] or asymptomatic unilateral hemodynamically significant [[ARAS]] in a viable kidney is not well known and clinically unrecognized (class 11b, LOE C)

2) [[Hypertension]]

*[[Percutaneous revascularization]] is used for patients with
*Hemodynamically significant [[renal artery stenosis]] along with accelerated [[hypertension]]
*[[Malignant hypertension]]
*[[Resistant hypertension]]
*In cases with [[hypertension]] and associated [[unilateral small kidney]].

3) Preservation of [[renal function]]

*[[Percutaneous revascularization]] is helpful in patients with [[ARAS]] + [[Chronic progressive kidney disease]] with [[bilateral renal artery stenosis]] or solitary functioning [[kidney]]. (Class IIa, LOE B)

*Also considered significant in [[patients]] with [[RAS]] and [[chronic renal insufficiency]] with [[unilateral renal artery stenosis]]. (Class IIb, LOE C)

4) Effects of [[renal artery stenosis]] on [[Congestive heart failure]] and [[unstable angina]]: [[Percutaneous revascularization]] is considered in [[patients]] with

*[[RAS]] + Recurrent [[congestive heart failure]] or sudden unexplained [[pulmonary edema]]. (Class I, LOE B)
*[[Patients]] with hemodynamically significant [[RAS]] along with [[unstable angina]] (Class IIa, LOE B)

 

===Percutaneous Transluminal Renal Angioplasty===
Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC)<ref name="pmid10749962">{{cite journal |vauthors=van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in 't Veld AJ, Schalekamp MA |title=The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis. Dutch Renal Artery Stenosis Intervention Cooperative Study Group |journal=N Engl J Med |volume=342 |issue=14 |pages=1007–14 |date=April 2000 |pmid=10749962 |doi=10.1056/NEJM200004063421403 |url=}}</ref> did a study to compare the effects of drug treatment and PTRA.

Despite the authors' claim that PTRA offered "little benefit" in comparison to pharmacological treatments, patients in the PTRA community were less likely over 12 months of follow-up to experience regression in their blood pressure regulation or renal artery occlusion.

===Renal Artery Stenting===

*Renal artery stenting is considered to be safe<ref name="pmid9715856">{{cite journal |vauthors=Dorros G, Jaff M, Mathiak L, Dorros II, Lowe A, Murphy K, He T |title=Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis |journal=Circulation |volume=98 |issue=7 |pages=642–7 |date=August 1998 |pmid=9715856 |doi=10.1161/01.cir.98.7.642 |url=}}</ref> and one of the effective<ref name="pmid9017938">{{cite journal |vauthors=Blum U, Krumme B, Flügel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M |title=Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty |journal=N Engl J Med |volume=336 |issue=7 |pages=459–65 |date=February 1997 |pmid=9017938 |doi=10.1056/NEJM199702133360702 |url=}}</ref> procedures involved in the management of renal artery stenosis.
*In a meta-analysis conducted in the past showed promising results with stent placement along with higher success rates (98% vs 77%) and less risk of restenosis (17% vs 26%)<ref name="pmid10887230">{{cite journal |vauthors=Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In 't Veld AJ |title=Stent placement for renal arterial stenosis: where do we stand? A meta-analysis |journal=Radiology |volume=216 |issue=1 |pages=78–85 |date=July 2000 |pmid=10887230 |doi=10.1148/radiology.216.1.r00jl0778 |url=}}</ref> as compared to what with PTRA.
*A randomized analysis revealed the effectiveness of renal stenting versus PTRA for rapid procedural success (88% versus 57%) and lower rates of restenosis (14 percent vs 48 percent, respectively) 70.
*In patients with ARAS and progressive renal insufficiency, other studies have indicated recovery or stability of renal function after unilateral or bilateral renal stenting..71,72
*After therapy with at least 2 antihypertensive drugs, in patients with ARAS and hypertension (blood pressure >140/90 mm Hg), renal stenting resulted in a 20 mm Hg decrease in systolic blood pressure and 1 less antihypertensive drug.73
*The ASTRAL<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> ( Angioplasty and Stenting for Renal Artery Lesions) and the STAR<ref name="pmid19907042">{{cite journal |vauthors=Wheatley K, Ives N, Gray R, Kalra PA, Moss JG, Baigent C, Carr S, Chalmers N, Eadington D, Hamilton G, Lipkin G, Nicholson A, Scoble J |title=Revascularization versus medical therapy for renal-artery stenosis |journal=N Engl J Med |volume=361 |issue=20 |pages=1953–62 |date=November 2009 |pmid=19907042 |doi=10.1056/NEJMoa0905368 |url=}}</ref> (Atherosclerotic Renal Artery Stenosis and Impaired Renal Function) trials, CORAL<ref name="pmid16824832">{{cite journal |vauthors=Cooper CJ, Murphy TP, Matsumoto A, Steffes M, Cohen DJ, Jaff M, Kuntz R, Jamerson K, Reid D, Rosenfield K, Rundback J, D'Agostino R, Henrich W, Dworkin L |title=Stent revascularization for the prevention of cardiovascular and renal events among patients with renal artery stenosis and systolic hypertension: rationale and design of the CORAL trial |journal=Am Heart J |volume=152 |issue=1 |pages=59–66 |date=July 2006 |pmid=16824832 |doi=10.1016/j.ahj.2005.09.011 |url=}}</ref> (Cardiovascular Outcomes in Renal Atherosclerotic Lesions) are the major trials conducted for analyzing the importance of renal artery stenting in the management of renal artery stenosis.

===Additional Interventional Procedures===
*While brachytherapy and cutting balloon atherotomy<ref name="pmid15152154">{{cite journal |vauthors=Jahraus CD, Meigooni AS |title=Vascular brachytherapy: a new approach to renal artery in-stent restenosis |journal=J Invasive Cardiol |volume=16 |issue=4 |pages=224–7; quiz (page following) |date=April 2004 |pmid=15152154 |doi= |url=}}</ref><ref name="pmid15553312">{{cite journal |vauthors=Otah KE, Alhaddad IA |title=Intravascular ultrasound-guided cutting balloon angioplasty for renal artery stent restenosis |journal=Clin Cardiol |volume=27 |issue=10 |pages=581–3 |date=October 2004 |pmid=15553312 |pmc=6654343 |doi=10.1002/clc.4960271012 |url=}}</ref> for renal artery in-stent restenosis have been used successfully, long-term findings are uncertain.

*Coronary drug-eluting stent usage<ref name="pmid15619320">{{cite journal |vauthors=Granillo GA, van Dijk LC, McFadden EP, Serruys PW |title=Percutaneous radial intervention for complex bilateral renal artery stenosis using paclitaxel eluting stents |journal=Catheter Cardiovasc Interv |volume=64 |issue=1 |pages=23–7 |date=January 2005 |pmid=15619320 |doi=10.1002/ccd.20240 |url=}}</ref> has also been identified for narrow renal arteries, but there is a shortage of well-designed trials to evaluate the adequate eluting drug dosage for this vessel

*The major drug-eluting stent is just 3.5 mm in diameter, which is an inappropriate dimension for stenting of a renal artery (with a normal diameter of 4-7 mm). In order to trap atherosclerotic debris and avoid distal embolization during renal stenting, 80 distal embolic safety systems have also been used, which may help maintain renal function.

===Surgery===
*Surgical revascularization<ref name="pmid6700670">{{cite journal |vauthors=White CW, Wright CB, Doty DB, Hiratza LF, Eastham CL, Harrison DG, Marcus ML |title=Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? |journal=N Engl J Med |volume=310 |issue=13 |pages=819–24 |date=March 1984 |pmid=6700670 |doi=10.1056/NEJM198403293101304 |url=}}</ref> is one of the effective modalities involved in the management of Renal artery stenosis. But the morbidity and mortality are higher with surgery as compared to stenting.

*In one of the few trials comparing ostial ARAS surgical revascularization with percutaneous revascularization, Balzer et al81 observed no substantial difference in long-term morbidity or mortality and no significant difference in blood pressure reduction.

*These findings show that surgical revascularization of ostial ARAS could be at least equal to PTRA. 

==References==