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| __NOTOC__
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| {{SK}} Acute kidney failure; acute renal failure; acute uremia; AKI; ARF
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| ==Overview==
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| Acute kidney injury (AKI), formerly known as acute renal failure, is characterized by an abrupt loss of kidney function resulting in a failure to excrete nitrogenous waste products (among others), and a disruption of fluid and electrolyte homeostasis. AKI defines a spectrum of disease with common clinical features including an increase in the serum creatinine and BUN levels, often associated with a reduction in urine volume. AKI can be caused by a multitude of factors broadly categorized into pre-renal (usually ischemic), intrinsic renal (usually toxic), and post-renal (usually obstructive) injuries. Generally, treatment is supportive until renal function is restored especially in light of the fluid overload, electrolyte imbalances, and uremic toxin accumulation. Still, renal replacement modalities are sometimes indicated.
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| ==Definition==
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| Over 30 different definitions of AKI have been used in the literature since it was first described, which prompted the need for a uniform definition. In 2002, The Acute Dialysis Quality Initiative (ADQI) proposed the first consensus definition known as the RIFLE criteria. The acronym combines a classification of 3 levels of renal dysfunction (Risk, Injury, Failure) with 2 clinical outcomes (Loss, ESRD). This unified classification was proposed to enable a viable comparison in trials of prevention and therapy and to observe clinical outcomes of the defined stages of AKI.<ref name="pmid15312219">{{cite journal| author=Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative workgroup| title=Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. | journal=Crit Care | year= 2004 | volume= 8 | issue= 4 | pages= R204-12 | pmid=15312219 | doi=10.1186/cc2872 | pmc=PMC522841 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15312219 }} </ref>
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| {| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
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| |+ '''''RIFLE criteria for the definition of acute kidney injury (AKI)'''''
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| | bgcolor="#d9ff54"|'''Classification''' || bgcolor="#d9ff54"|'''GFR criteria''' || bgcolor="#d9ff54"|'''Urine output criteria'''
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| | bgcolor="#ececec"|'''R'''isk || 1.5x increase in SCr or GFR decrease >25% || <0.5 mL/kg/h for 6 hours
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| | bgcolor="#ececec"|'''I'''njury || 2x increase in SCr or GFR decrease >50%|| <0.5 mL/kg/h for 12 hours
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| | bgcolor="#ececec"|'''F'''ailure || 3x increase in SCr or GFR decrease >75% || <0.3 mL/kg/h for 24 hours or anuria for 12 hours
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| | bgcolor="#ececec"|'''L'''oss || colspan="2"| Complete loss of renal function >4 weeks | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=vnTR_y3Sf-k|350}} |
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| | bgcolor="#ececec"|'''E'''nd-stage Renal Disease || colspan="2"|Complete loss of renal function >3 months
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| In 2007, the Acute Kidney Injury Network (AKIN) proposed a modified diagnostic criteria based on the RIFLE criteria. The initiative separated the definition and staging into 2 separate entities previously combined in the RIFLE criteria. This made the definition more clinically applicable. AKI was defined as either one of the following:<ref name="pmid17331245">{{cite journal| author=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG et al.| title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. | journal=Crit Care | year= 2007 | volume= 11 | issue= 2 | pages= R31 | pmid=17331245 | doi=10.1186/cc5713 | pmc=PMC2206446 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17331245 }} </ref>
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| * '''an increase in serum creatinine by 0.3 mg/dL in 48 hours'''
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| * '''an increase in serum creatinine by more than 50% of baseline or 1.5 times baseline occuring in the past 7 days'''
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| * '''a decrease in urine volume <0.5 mL/kg/h for 6 hours'''
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| |}
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| In March 2012, the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for Acute Kidney Injury retained the AKIN definition while implementing modifications to the staging criteria of AKI. <ref name="doi10.1038/kisup.2011.34">{{cite journal|author=Kidney Disease Improving Global Outcomes Work Group| title=2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury| journal=Kidey Int Supp |year= 2012 | volume= 2 | pages= 69-88 | doi=10.1038/kisup.2011.34 | pmc= |url=http://www.nature.com/kisup/journal/v2/n1/full/kisup201134a.html }} </ref>
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| ==Historical Perspective==
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| It is really unclear when acute kidney injury or acute renal failure came to light as a separate disease entity. The first documented report of abrupt loss of renal function came from Beall et al in 1941 who described a man admitted to St. Thomas's Hospital after a crush injury to the leg in a bombing incident. They describe a course of rapidly progressive renal insufficiency with dark urine, edema, elevated potassium levels, and disorientation. <ref name="pmid20783578">{{cite journal| author=Beall D, Bywaters EG, Belsey RH, Miles JA| title=Crush Injury with Renal Failure. | journal=Br Med J | year= 1941 | volume= 1 | issue= 4185| pages= 432-4 | pmid=20783578 | doi= | pmc=PMC2161708 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20783578 }} </ref>
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| The earliest definition came from Lucké in 1946 who described the histologic pathology we now know as acute tubular necrosis. The term ''lower nephron nephrosis'' was introduced and was later used to refer to abrupt renal failure secondary to excessive vomiting, thermal burns, crush injuries, hemolysis, and obstructive prostate disease.<ref name="pmid20276793">{{cite journal| author=LUCKE B| title=Lower nephron nephrosis; the renal lesions of the crush syndrome, of burns, transfusions, and other conditions affecting the lower segments of the nephrons. | journal=Mil Surg | year= 1946 | volume= 99 | issue= 5 | pages= 371-96 |pmid=20276793 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20276793}} </ref><ref name="pmid18892579">{{cite journal| author=STRAUSS MB| title=Acute renal insufficiency due to lower-nephron nephrosis. | journal=N Engl J Med |year= 1948 | volume= 239 | issue= 19 | pages= 693-700 | pmid=18892579 | doi=10.1056/NEJM194811042391901 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18892579 }} </ref> The term slowly drifted to become acute renal failure to depict a clinical syndrome rather than a pathologic finding. Acute renal failure was then replaced by acute kidney injury in 2006 following a consensus that even minor changes in serum creatinine not necessarily overt failure can lead to significant changes in outcome.
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| ==Staging==
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| Initially, the staging of AKI was a part of the proposed definition by the ADQI initiative and the RIFLE criteria. In 2007, AKIN proposed separated the 2 and created a new staging scheme modified from the RIFLE criteria. Prior to the 2012, RIFLE and AKIN criteria were used interchangeably to stage patients with renal injury.<ref name="pmid15312219">{{cite journal|author=Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative workgroup| title=Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. | journal=Crit Care | year= 2004 | volume= 8 | issue= 4 | pages= R204-12 | pmid=15312219 | doi=10.1186/cc2872 | pmc=PMC522841 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15312219 }} </ref><ref name="pmid17331245">{{cite journal| author=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG et al.|title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. | journal=Crit Care | year= 2007 | volume= 11 | issue= 2| pages= R31 | pmid=17331245 | doi=10.1186/cc5713 | pmc=PMC2206446 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17331245 }} </ref> Although certain concerns about the differences between the 2 classification schemes, it was shown that the differences do not carry through to mortality and outcome measures.<ref name="pmid18281319">{{cite journal| author=Bagshaw SM, George C, Bellomo R, ANZICS Database Management Committe| title=A comparison of the RIFLE and AKIN criteria for acute kidney injury in critically ill patients. | journal=Nephrol Dial Transplant | year= 2008 | volume= 23 | issue= 5 | pages= 1569-74 | pmid=18281319 | doi=10.1093/ndt/gfn009 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18281319 }} </ref>
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| {| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
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| |+ '''''Modified RIFLE staging scheme for acute kidney injury according to the Acute Kidney Injury Network (AKIN).'''''
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| | bgcolor="#d9ff54"|'''Classification''' || bgcolor="#d9ff54"|'''GFR criteria''' || bgcolor="#d9ff54"|'''Urine output criteria'''
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| | bgcolor="#ececec"|'''Stage 1''' || Increase in SCr ≥0.3 mg/dL or 1.5x to 2x increase from baseline || <0.5 mL/kg/h for 6 hours
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| | bgcolor="#ececec"|'''Stage 2''' || 2x to 3x increase in SCr from baseline || <0.5 mL/kg/h for 12 hours
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| | bgcolor="#ececec"|'''Stage 3''' || >3x increase in SCr or SCr≥ 4.0 mg/dL with acute increase >0.5 md/dL || <0.3 mL/kg/h for 24 hours or anuria for 12 hours
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| |}
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| In 2012, the KDIGO AKI guidelines proposed a combined staging scheme that takes into account both criteria and clinical outcome. <ref name="doi10.1038/kisup.2011.34">{{cite journal|author=Kidney Disease Improving Global Outcomes Work Group| title=2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury| journal=Kidey Int Supp |year= 2012 | volume= 2 | pages= 69-88 |doi=10.1038/kisup.2011.34 | pmc=|url=http://www.nature.com/kisup/journal/v2/n1/full/kisup201134a.html }} </ref> The rationale behind AKI staging is the needed to determine overall outcome as higher stags of AKI carry a greater risk of all cause and cardiovascular mortality, renal replacement, as well as chronic kidney disease even after AKI resolution.<ref name="pmid16715038">{{cite journal| author=Uchino S, Bellomo R, Goldsmith D, Bates S, Ronco C| title=An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. | journal=Crit Care Med | year= 2006 | volume= 34 | issue= 7 | pages= 1913-7 | pmid=16715038 | doi=10.1097/01.CCM.0000224227.70642.4F | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16715038 }} </ref><ref name="pmid17962378">{{cite journal| author=Bagshaw SM, George C, Dinu I, Bellomo R| title=A multi-centre evaluation of the RIFLE criteria for early acute kidney injury in critically ill patients. | journal=Nephrol Dial Transplant | year= 2008 | volume= 23 | issue= 4 | pages= 1203-10 | pmid=17962378 | doi=10.1093/ndt/gfm744 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17962378 }} </ref><ref name="pmid18160961">{{cite journal| author=Ricci Z, Cruz D, Ronco C| title=The RIFLE criteria and mortality in acute kidney injury: A systematic review. | journal=Kidney Int | year= 2008 | volume= 73 | issue= 5 | pages= 538-46 | pmid=18160961 | doi=10.1038/sj.ki.5002743 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18160961 }} </ref><ref name="pmid17314324">{{cite journal| author=Ali T, Khan I, Simpson W, Prescott G, Townend J, Smith W et al.| title=Incidence and outcomes in acute kidney injury: a comprehensive population-based study. | journal=J Am Soc Nephrol | year= 2007 | volume= 18 | issue= 4 | pages= 1292-8 | pmid=17314324 | doi=10.1681/ASN.2006070756 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17314324 }} </ref>
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| {| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
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| |+ '''''2012 KDIGO AKI Guidelines - Proposed staging criteria for AKI modified from AKIN'''''
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| | bgcolor="#d9ff54"|'''Staging''' || bgcolor="#d9ff54"|'''GFR criteria''' || bgcolor="#d9ff54"|'''Urine output criteria'''
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| | bgcolor="#ececec"|'''Stage 1''' || 1.5 - 1.9 times baseline or ≥ 0.3 mg/dl increase || <0.5 ml/kg/h for 6 - 12 hours
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| | bgcolor="#ececec"|'''Stage 2''' || 2.0 - 2.9 times baseline || <0.5 ml/kg/h for ≥ 12 hours | | | [[File:Siren.gif|link=Acute kidney failure resident survival guide|41x41px]]|| <br> || <br> |
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| | | [[Acute kidney failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| | bgcolor="#ececec"|'''Stage 3''' || 3.0 times baseline <br> '''or''' increase in serum creatinine to 4.0 mg/dL <br> '''or''' initiation of renal replacement therapy <br> '''or''' decrease in eGFR to <35 ml/min per 1.73 m<sup>2</sup> (in patients <18 years) || <0.3 mL/kg/h for 24 hours <br> '''or''' anuria for 12 hours | |
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| | {{Acute kidney injury}} |
| | {{CMG}} {{AE}} {{SSK}}, {{F.K}} |
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| The guidelines also advocated that in case of discordance between urine output and serum creatinine patients should be classified to the highest applicable AKI stage. Also, new emphasis on the differences seen in the pediatric population gave rise to revised definition of Stage 3 AKI in patients less than 18 years of age.<ref name="doi10.1038/kisup.2011.34">{{cite journal|author=Kidney Disease Improving Global Outcomes Work Group| title=2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury| journal=Kidey Int Supp |year= 2012 | volume= 2 | pages= 69-88 |doi=10.1038/kisup.2011.34 | pmc= |url=http://www.nature.com/kisup/journal/v2/n1/full/kisup201134a.html }} </ref>
| | {{SK}} Acute kidney failure; acute renal failure; acute uremia; AKI; ARF; uremia, |
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| ==Pathophysiology & Etiologies==
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| Etiologies of AKI can be divided based on pathophysiologic mechanisms into 3 broad categories: prerenal, intrinsic renal, and postrenal causes.
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| [[Image:Etiologies_of_AKI.jpg|1000px|center|border]]
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| ===Prerenal AKI===
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| Prerenal AKI, known as prerenal azotemia, is by far the most common cause of AKI representing 30-50% of all cases. It is provoked by inadequate renal blood flow commonly due to decreased effective circulating blood flow. This causes a decrease in the intraglomerular hydrostatic pressure required to achieve proper glomerular filtration.
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| [[Image:PrerenalAKI.jpg|500px|border|center]]
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| Blood flow to the kidneys can vary with systemic changes; however, glomerular perfusion pressure and GFR are maintained relatively constant by the kidney itself. Under physiologic conditions, minor drops in blood flow to the renal circulation are counteracted by changes in the resistances across the afferent and efferent arterioles of individual glomerular capillary beds.<ref name="pmid16603656">{{cite journal| author=Loutzenhiser R, Griffin K, Williamson G, Bidani A| title=Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms. | journal=Am J Physiol Regul Integr Comp Physiol | year= 2006 | volume= 290 | issue= 5 | pages= R1153-67 | pmid=16603656 | doi=10.1152/ajpregu.00402.2005 | pmc=PMC1578723 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16603656 }} </ref> The afferent arteriole vasodilates via 2 mechanisms.<ref name="pmid3045546">{{cite journal| author=Badr KF, Ichikawa I| title=Prerenal failure: a deleterious shift from renal compensation to decompensation. | journal=N Engl J Med | year= 1988 | volume= 319 | issue= 10 | pages= 623-9 | pmid=3045546 | doi=10.1056/NEJM198809083191007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3045546 }} </ref> The myogenic reflex, mediating medial smooth muscle relaxation in states of decrease perfusion pressure, vasodilates the afferent arteriole leading to increased blood flow.<ref name="pmid17229679">{{cite journal| author=Cupples WA, Braam B| title=Assessment of renal autoregulation. | journal=Am J Physiol Renal Physiol | year= 2007 | volume= 292 | issue= 4 | pages= F1105-23 | pmid=17229679 | doi=10.1152/ajprenal.00194.2006 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17229679 }} </ref> Additionally, intrarenal synthesis of vasodilatory prostaglandins such as prostacyclin and prostaglandin E2 causes further dilation of the afferent arteriole.<ref name="pmid4355037">{{cite journal| author=Herbaczynska-Cedro K, Vane JR| title=Contribution of intrarenal generation of prostaglandin to autoregulation of renal blood flow in the dog. | journal=Circ Res | year= 1973 | volume= 33 | issue= 4 | pages= 428-36 | pmid=4355037 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4355037 }} </ref> The mechanism explains why the intake of NSAIDs leads to acute kidney injury by inhibiting this autoregulatory mechanism.<ref name="pmid19028206">{{cite journal| author=Winkelmayer WC, Waikar SS, Mogun H, Solomon DH| title=Nonselective and cyclooxygenase-2-selective NSAIDs and acute kidney injury. | journal=Am J Med | year= 2008 | volume= 121 | issue= 12 | pages= 1092-8 | pmid=19028206 | doi=10.1016/j.amjmed.2008.06.035 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19028206 }} </ref>
| | ==[[Acute kidney injury overview|Overview]]== |
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| | ==[[Acute kidney injury historical perspective|Historical Perspective]]== |
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| At the level of the efferent arteriole, an increase in resistance is crucial for appropriate maintenance of glomerular hydrostatic pressure. This is achieved by an increase in the production of angiotensin II (via the Renin-Angiotensin System) which acts preferentially on the efferent arteriole leading to vasoconstriction.<ref name="pmid9892156">{{cite journal| author=Arendshorst WJ, Brännström K, Ruan X| title=Actions of angiotensin II on the renal microvasculature. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 Suppl 11 | issue= | pages= S149-61 | pmid=9892156 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9892156 }} </ref> Important medications that target angiotensin II production and action are ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) which may be responsible for renal decompensation in patients dependent on the action of angiotensin II to maintain glomerular perfusion pressure. Such is the case in chronic kidney disease patients, whose autoregulatory mechanisms are typically operating at maximum capacity.<ref name="pmid17715412">{{cite journal| author=Abuelo JG| title=Normotensive ischemic acute renal failure. | journal=N Engl J Med | year= 2007 | volume= 357 | issue= 8 | pages= 797-805 | pmid=17715412 | doi=10.1056/NEJMra064398 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17715412 }} </ref>
| | ==[[Acute kidney injury classification|Classification]]== |
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| | ==[[Acute kidney injury pathophysiology|Pathophysiology]]== |
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| As such, the pathophysiology of prerenal azotemia entails a drop in renal plasma flow beyond the capacity of autoregulation, a blunted or inadequate renal compensation for an otherwise tolerable change in perfusion, or a combination of both. This eventually leads to ischemic renal injury particularly to the medulla which is maintained in hypoxic conditions at baseline. Causes of prerenal injury are summarized in the figure below. To note, as prerenal AKI progresses with further ischemia, it transforms into acute tubular necrosis (ATN) crossing into the realm of intrinsic AKI.
| | ==[[Acute kidney injury causes|Causes]]== |
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| | ==[[Acute kidney injury differential diagnosis|Differentiating Acute kidney injury from other Diseases]]== |
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| [[Image:Prerenal_causes.png|800px|center]] | | ==[[Acute kidney injury epidemiology and demographics|Epidemiology and Demographics]]== |
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| ===Intrinsic Renal AKI=== | | ==[[Acute kidney injury risk factors|Risk Factors]]== |
| Intrinsic renal AKI generally occurs due to renal parenchymal injury and may be classified according to the site of injury into: glomerular, tubular, interstitial, and vascular.
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| ====Tubular AKI==== | | ==[[Acute kidney injury screening|Screening]]== |
| The most common form of intrinsic renal AKI involves damage to the renal tubules. In this context, the most common etiologies are sepsis, nephrotoxins, and ischemia. Ischemic AKI is part of a disease continuum involving prerenal AKI and manifests in states of prolonged renal blood flow compromise or renal hypoperfusion with other pre-existing or concomitant renal insults. Although sometimes dubbed acute tubular necrosis (ATN), ATN is non-specific to prerenal disease, and may be induced by sepsis and nephrotoxins. ATN is also not a very accurate pathological term, as renal biopsies have rarely shown true tubular necrosis, but rather tubular cell injury & apoptosis with secondary dysfunction are more accurate. These pathological manifestations are related to hypoxia and ATP depletion in areas that are physiologically hypoxic such as the renal medulla, and areas that are very metabolically active such as the proximal tubule. The response of the renal tubules and the microvasculature are maladaptive leading to a paradoxical increase in hypoxia and further damage and inflammation.<ref name="pmid12874476">{{cite journal| author=Bonventre JV, Weinberg JM| title=Recent advances in the pathophysiology of ischemic acute renal failure. |journal=J Am Soc Nephrol | year= 2003 | volume= 14 | issue= 8 | pages= 2199-210 | pmid=12874476 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12874476 }} </ref> Ischemia and hypoxia are known to cause increased reactivity to vasoconstrictive agents, and decreased vasodilatory responses in arterioles as compared to normal kidneys.<ref name="pmid8528754">{{cite journal| author=Conger JD, Weil JV| title=Abnormal vascular function following ischemia-reperfusion injury. | journal=J Investig Med | year= 1995 | volume= 43 | issue= 5 | pages= 431-42 | pmid=8528754 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8528754 }} </ref>
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| [[Image:Hypoxia_AKI.jpg|650px|border|center]]
| | ==[[Acute kidney injury natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| AKI is seen in 20 to 25% of cases of sepsis and in 50% of cases of septic shock. A decrease in GFR in a septic patient is usually a marker of poor prognosis, and the combination of sepsis and AKI is associated with a mortality rate of 70%. Although most cases of AKI occur with severe hemodynamic compromise in septic patients, renal injury may occur without overt hypotension. While there is clear tubular damage in sepsis-associated AKI, interstitial inflammation and interstitial edema have also been proposed in the pathogenesis.<ref name="pmid16707563">{{cite journal| author=Devarajan P| title=Update on mechanisms of ischemic acute kidney injury. | journal=J Am Soc Nephrol | year= 2006 | volume= 17 | issue= 6 | pages= 1503-20 | pmid=16707563 | doi=10.1681/ASN.2006010017 |pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16707563 }} </ref><ref name="pmid20427950">{{cite journal| author=Bonventre JV| title=Pathophysiology of AKI: injury and normal and abnormal repair. | journal=Contrib Nephrol | year= 2010 | volume= 165 | issue= | pages= 9-17 | pmid=20427950 | doi=10.1159/000313738 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20427950 }} </ref> The mechanisms of alteration of renal hemodynamics proposed in sepsis include excessive efferent arteriolar vasodilation or generalized renal vasoconstriction secondary to tumor necrosis factor induced release of endothelin.
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| Another major cause of intrinsic renal AKI is nephrotoxins. The latter may be either endogenous such as myoglobin, hemoglobin, and myeloma light chains, or exogenous such as contrast agents, antibiotics, and chemotherapeutic agents. The kidney is a particularly susceptible organ to toxin injury mainly due to the high blood perfusion and the high concentration of substances in the kidneys destined for excretion. Nephrotoxic injury may be secondary to tubular, interstitial, or microvascular damage depending on the nephrotoxin itself. Major risk factors for nephrotoxic AKI include old age, pre-existing chronic kidney disease (CKD), and prerenal azotemia.<ref name="pmid16932399">{{cite journal| author=Choudhury D, Ahmed Z| title=Drug-associated renal dysfunction and injury.| journal=Nat Clin Pract Nephrol | year= 2006 | volume= 2 | issue= 2 | pages= 80-91 | pmid=16932399 | doi=10.1038/ncpneph0076 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16932399 }} </ref>
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| Contrast induced nephropathy (CIN) recently called contrast induced AKI (CIAKI) is also major cause of intrinsic injury caused by iodinated contrast media used in cardiovascular imaging. This entity is virtually non-existent in healthy young individuals. Risk factors that increase susceptibility to contrast media include advanced age, pre-existing CKD, diabetic nephropathy, severe cardiac failure, and concomitant exposure to other nephrotoxins. The pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism. It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process. The most important mechanism thought to be involved in CIN is a reduction in renal perfusion at the level of the microvasculature leading to tubular damage. This is attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure. Studies have also proposed injury to renal tubular cells may occur via a direct cytotoxic effect of the contrast media and via reactive oxygen species production.<ref name="pmid21784541">{{cite journal| author=Wong PC, Li Z, Guo J, Zhang A| title=Pathophysiology of contrast-induced nephropathy. | journal=Int J Cardiol | year= 2012 | volume= 158 | issue= 2 | pages= 186-92 | pmid=21784541 | doi=10.1016/j.ijcard.2011.06.115 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21784541 }} </ref>
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| [[Image:Nephrotoxins.jpg|center]] | |
| ====Glomerular & Vascular AKI====
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| Glomerular damage causing AKI accounts for a small propotion of cases of AKI. Glomerulonephritis leading to AKI is usually seen in rapidly progressive glomerulonephritis (RPGN). Other forms of glomerulonephritis progress slowly and generally lead to chronic kidney disease. RPGN is characterized by a triad of hematuria, proteinuria, and hypertension progressing to a decrease in GFR and urine output.<ref name="pmid10688410">{{cite journal| author=Erwig LP, Rees AJ|title=Rapidly progressive glomerulonephritis. | journal=J Nephrol | year= 1999 | volume= 12 Suppl 2 | issue= | pages= S111-9 | pmid=10688410 | doi= | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10688410 }} </ref> RPGN can be idiopathic or secondary to SLE, Henoch Schonlein Purpura, Wegener’s Granulomatosis, and Goodpasture’s Syndrome. The pathophysiology is almost always related to an autoimmune insult, but specific characteristics depend on the underlying etiologies.<ref name="pmid23689582">{{cite journal| author=Chen YX, Chen N|title=Pathogenesis of rapidly progressive glomerulonephritis: what do we learn? | journal=Contrib Nephrol | year= 2013 | volume= 181 | issue= | pages= 207-15 |pmid=23689582 | doi=10.1159/000348633 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23689582 }} </ref>
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| Other causes of AKI of vascular origin include diseases affecting the macro and microvasculature not only confined to the glomerular capillaries. Examples include TTP/HUS & DIC associated with microangiopathic hemolytic anemia (MAHA) typically arising from an endothelial cell injury with subsequent leukocyte adhesion, complement consumption, platelet aggregation and eventual ischemic damage. Other causes include atheroemboli, calcineurin inhibitors in renal transplant patients via vasoconstriction of the afferent arterioles (although a tubulointerstitial pattern is also seen),<ref name="pmid19218475">{{cite journal| author=Naesens M, Kuypers DR, Sarwal M| title=Calcineurin inhibitor nephrotoxicity. | journal=Clin J Am Soc Nephrol | year= 2009 | volume= 4 | issue= 2 | pages= 481-508 | pmid=19218475 | doi=10.2215/CJN.04800908 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19218475 }} </ref> and vasculitides.<ref name="pmid11532079">{{cite journal| author=Ruggenenti P, Noris M, Remuzzi G| title=Thrombotic microangiopathy, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura. | journal=Kidney Int | year= 2001| volume= 60 | issue= 3 | pages= 831-46 | pmid=11532079 | doi=10.1046/j.1523-1755.2001.060003831.x | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11532079 }} </ref>
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| ====Interstitial AKI====
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| AKI may be secondary to acute interstitial nephritis caused by an idiosyncratic immune-mediated mechanism. Classically it is associated with a number of medications including penicillins, cephalosporins, NSAIDs, sulfonamides, and allopurinol. AIN can also be secondary to an infectious process, or systemic syndromes such as cryoglobulinemia, Sjogren syndrome, sarcoidosis, and primary biliary cirrhosis. Clinically, it may be associated with fever, and urinary eosinophilia although it may often be asymptomatic. Pathophysiology involves a cell-mediated immune reaction with interstitial infiltrates mostly composed of lymphocytes, macrophages, eosinophils, and plasma cells, with subsequent transformation into areas of interstitial fibrosis.<ref name="pmid11532079">{{cite journal| author=Ruggenenti P, Noris M, Remuzzi G| title=Thrombotic microangiopathy, hemolytic uremic syndrome, and thrombotic thrombocytopenic purpura. |journal=Kidney Int | year= 2001 | volume= 60 | issue= 3 | pages= 831-46 | pmid=11532079 | doi=10.1046/j.1523-1755.2001.060003831.x | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11532079 }} </ref>
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| ===Postrenal AKI===
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| Postrenal AKI occurs due to an obstruction in the urinary flow leading to an increase in the intratubular hydrostatic pressure which interferes with proper glomerular filtration. Obstructions occurring at the level of the renal pelvis and the ureters must affect both kidneys simultaneously to cause AKI in healthy adults unless only one kidney is functional. Causes of upper tract obstructions may be intraluminal such as calculi or blood clots, transmural secondary to neoplastic invasion, or extrinsic compression by retroperitoneal fibrosis, neoplasia, or an abscess. The most common cause of postrenal AKI is bladder neck obstruction secondary to benign prostatic hypertrophy and prostate cancer. Other etiologies of lower urinary tract obstruction are calculi, blood clots and strictures. Patients usually have evident hydronephrosis unless early in the course of obstruction. <ref name="pmid17495862">{{cite journal| author=Patel TV, Kumar S, Singh AK| title=Post-renal acute renal failure. | journal=Kidney Int | year= 2007 | volume= 72 | issue= 7 | pages= 890-4 | pmid=17495862 | doi=10.1038/sj.ki.5002301 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17495862 }} </ref>
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| ==Epidemiology and Demographics==
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| ===AKI in the General Population===
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| ===AKI in ICU Patients===
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| ==Risk Factors==
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| ==Differential Diagnosis==
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| ==Natural History, Complications & Prognosis==
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| ==Diagnosis== | | ==Diagnosis== |
| ===History===
| | [[Acute kidney injury diagnostic study of choice|Diagnostic study of choice]] | [[Acute kidney injury history and symptoms|History and Symptoms]] | [[Acute kidney injury physical examination|Physical Examination]] | [[Acute kidney injury laboratory findings|Laboratory Findings]] | [[Acute kidney injury electrocardiogram|Electrocardiogram]] | [[Acute kidney injury x ray|X-Ray Findings]] | [[Acute kidney injury echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[A cute kidney injuryCT scan|CT-Scan Findings]] | [[Acute kidney injury MRI|MRI Findings]] | [[Acute kidney injury other imaging findings|Other Imaging Findings]] | [[Acute kidney injury other diagnostic studies|Other Diagnostic Studies]] |
| ===Physical Exam===
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| ===Lab findings===
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| ===Novel Biomarkers===
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| ==Treatment== | | ==Treatment== |
| ===Medical Therapy===
| | [[Acute kidney injury medical therapy|Medical Therapy]] | [[Acute kidney injury interventions|Interventions]] | [[Acute kidney injury surgery|Surgery]] | [[Acute kidney injury primary prevention|Primary Prevention]] | [[Acute kidney injury secondary prevention|Secondary Prevention]] | [[Acute kidney injury cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Acute kidney injury future or investigational therapies|Future or Investigational Therapies]] |
| ===Renal Replacement Therapy===
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| ===Prophylaxis===
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| ===Future or Investigational Therapies===
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| ==AKI and Chronic Kidney Disease==
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| ==See also== | | ==Case Studies== |
| * [[BUN-to-creatinine ratio]]
| | [[Acute kidney injury case study one|Case #1]] |
| * [[Chronic kidney disease]]
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| * [[Dialysis]]
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| * [[Renal failure]]
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| * [[Rhabdomyolysis]]
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| * [[Contrast-induced nephropathy]]
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| ==Related Chapters==
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| *[[Chronic renal failure|Chronic Renal Failure]]
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| *[[Dialysis]]
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| *[[Hepatorenal syndrome|Hepatorenal Syndrome]]
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| *[[Renal failure|Renal Failure]]
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| ==References==
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| {{Reflist|2}}
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| {{Nephrology}} | | {{Nephrology}} |
| {{Organ failure}} | | {{Organ failure}} |
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| [[Category:Causes of death]]
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| [[Category:Emergency medicine]] | | [[Category:Emergency medicine]] |
| [[Category:Intensive care medicine]]
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| [[Category:Kidney diseases]]
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| [[Category:Medical emergencies]]
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| [[Category:Medicine]] | | [[Category:Medicine]] |
| [[Category:Nephrology]] | | [[Category:Nephrology]] |
| [[Category:Organ failure]] | | [[Category:Up-To-Date]] |
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| {{WH}} | | {{WH}} |
| {{WS}} | | {{WS}} |
