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__NOTOC__ | __NOTOC__ | ||
{{Renal artery stenosis}} | {{Renal artery stenosis}} | ||
{{CMG}} | {{CMG}} {{AE}} {{Shivam Singla}} | ||
==Overview== | ==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== | |||
Latest revision as of 07:33, 8 April 2021
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Renal artery stenosis Microchapters |
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Renal artery stenosis overview On the Web |
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American Roentgen Ray Society Images of Renal artery stenosis overview |
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Risk calculators and risk factors for Renal artery stenosis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[2]
Overview
- 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 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 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