Acute kidney injury: Difference between revisions

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__NOTOC__
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{{SI}}
{{CMG}}
 
{{SK}} Acute kidney failure; acute renal failure; acute uremia; AKI; ARF
 
==Overview==
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.
 
==Definition==
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>
 
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
|+ '''''RIFLE criteria for the definition of acute kidney injury (AKI)'''''
| bgcolor="#d9ff54"|'''Classification''' ||  bgcolor="#d9ff54"|'''GFR criteria''' ||  bgcolor="#d9ff54"|'''Urine output criteria'''
|-
|-
| bgcolor="#ececec"|'''R'''isk || 1.5x increase in SCr or GFR decrease >25% || <0.5 mL/kg/h for 6 hours
| {{#ev:youtube|https://https://www.youtube.com/watch?v=vnTR_y3Sf-k|350}}
|-
|-
| bgcolor="#ececec"|'''I'''njury || 2x increase in SCr or GFR decrease >50%|| <0.5 mL/kg/h for 12 hours
|-
| 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
|-
| bgcolor="#ececec"|'''L'''oss || colspan="2"| Complete loss of renal function >4 weeks
|-
| bgcolor="#ececec"|'''E'''nd-stage Renal Disease || colspan="2"|Complete loss of renal function >3 months
|}
|}
 
__NOTOC__
 
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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>
 
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center"
|+
| bgcolor="#d9ff54"|
 
* '''an increase in serum creatinine by 0.3 mg/dL in 48 hours'''
 
* '''an increase in serum creatinine by more than 50% of baseline or 1.5 times baseline occuring in the past 7 days'''
 
* '''a decrease in urine volume <0.5 mL/kg/h for 6 hours'''
|}
 
 
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>
 
==Historical Perspective==
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>
 
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.
 
==Staging==
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>
 
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
|+ '''''Modified RIFLE staging scheme for acute kidney injury according to the Acute Kidney Injury Network (AKIN).'''''
| bgcolor="#d9ff54"|'''Classification''' || bgcolor="#d9ff54"|'''GFR criteria''' || bgcolor="#d9ff54"|'''Urine output criteria'''
|-
| 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
|-
| bgcolor="#ececec"|'''Stage 2''' || 2x to 3x increase in SCr from baseline || <0.5 mL/kg/h for 12 hours
|-
| 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
|}
 
 
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>
 
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
|+ '''''2012 KDIGO AKI Guidelines - Proposed staging criteria for AKI modified from AKIN'''''
| bgcolor="#d9ff54"|'''Staging''' || bgcolor="#d9ff54"|'''GFR criteria''' || bgcolor="#d9ff54"|'''Urine output criteria'''
|-
| 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
|-
| bgcolor="#ececec"|'''Stage 2''' || 2.0 - 2.9 times baseline || <0.5 ml/kg/h for ≥ 12 hours
|-
|-
| 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
| [[File:Siren.gif|link=Acute kidney failure resident survival guide|41x41px]]|| <br> || <br>
| [[Acute kidney failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
|}
|}


{{Acute kidney injury}}
{{CMG}} {{AE}} {{SSK}}, {{F.K}}


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,
 
==Pathophysiology & Etiologies==
Etiologies of AKI can be divided based on pathophysiologic mechanisms into 3 broad categories: prerenal, intrinsic renal, and postrenal causes.


==[[Acute kidney injury overview|Overview]]==


[[Image:Etiologies_of_AKI.jpg|1000px|center|border]]
==[[Acute kidney injury historical perspective|Historical Perspective]]==


===Prerenal AKI===
==[[Acute kidney injury classification|Classification]]==
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.


[[Image:PrerenalAKI.jpg|500px|border|center]]
==[[Acute kidney injury pathophysiology|Pathophysiology]]==


==[[Acute kidney injury causes|Causes]]==


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 differential diagnosis|Differentiating Acute kidney injury from other Diseases]]==


==[[Acute kidney injury epidemiology and demographics|Epidemiology and Demographics]]==


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 risk factors|Risk Factors]]==


==[[Acute kidney injury screening|Screening]]==


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 natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
 
 
[[Image:Prerenal_causes.png|800px|center]]
 
===Intrinsic Renal AKI===
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.
 
====Tubular AKI====
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>
 
[[Image:Hypoxia_AKI.jpg|650px|border|center]]
 
 
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.
 
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>
 
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>
 
[[Image:Nephrotoxins.jpg|center]]
====Glomerular & Vascular AKI====
 
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>
 
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>
 
====Interstitial AKI====
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>
 
===Postrenal AKI===
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>
 
==Epidemiology and Demographics==
===AKI in the General Population===
Most studies addressing the epidemiology of AKI focus on patients admitted to the hospital due to the high incidence of AKI in that setting. Ali el al conducted a retrospective cohort study in the Grampian region of Scotland involving 523,390 subjects for a span of 6 months. Their results showed an overall 6-month incidence of approximately 0.09% in the general population. The estimated yearly incidence was 1811 pmp for AKI without prior history of kidney disease. Out of the patients with AKI, 53% were males, 67.7% had full renal recovery, and 7.8% required renal replacement therapy. To note, the in-hospital mortality was estimated to be 32.7% while the 6-month mortality approached 50%. <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>
 
===AKI in ICU Patients===
Many studies have addressed the epidemiology of AKI in the intensive care unit with varying incidence rates. A trend of increasing incidence of is apparent with reported incidence of 4.9% in 1983, 7.2% in 2002, and up to 67% most recently.<ref name="pmid6824004">{{cite journal| author=Hou SH, Bushinsky DA, Wish JB, Cohen JJ, Harrington JT| title=Hospital-acquired renal insufficiency: a prospective study. | journal=Am J Med | year= 1983 | volume= 74 | issue= 2 | pages= 243-8 | pmid=6824004 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6824004 }} </ref><ref name="pmid11979336‎">{{cite journal| author=Nash K, Hafeez A, Hou S| title=Hospital-acquired renal insufficiency. | journal=Am J Kidney Dis | year= 2002 | volume= 39 | issue= 5 | pages= 930-6 | pmid=11979336‎ | doi=10.1053/ajkd.2002.32766 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11979336 }} </ref>  Thakar et al reported an overall AKI incidence of 22% when studying 323,395 ICU patients admitted to the ICU in Veterans Affairs Hospitals across the USA, 17.5% of which matched the criteria for Stage 1 AKI.<ref name="pmid19602973">{{cite journal| author=Thakar CV, Christianson A, Freyberg R, Almenoff P, Render ML| title=Incidence and outcomes of acute kidney injury in intensive care units: a Veterans Administration study. | journal=Crit Care Med | year= 2009 | volume= 37 | issue= 9 | pages= 2552-8 | pmid=19602973 | doi=10.1097/CCM.0b013e3181a5906f | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19602973 }} </ref>  The NEiPHROS-AKI study prospectively assessed the incidence rates of AKI in 19 ICUs in northeastern Italy in a 3-month period following the RIFLE criteria and showed a lower incidence of 10.8% in the cohort of 2164 patients.<ref name="pmid17699446">{{cite journal| author=Cruz DN, Bolgan I, Perazella MA, Bonello M, de Cal M, Corradi V et al.| title=North East Italian Prospective Hospital Renal Outcome Survey on Acute Kidney Injury (NEiPHROS-AKI): targeting the problem with the RIFLE Criteria. | journal=Clin J Am Soc Nephrol | year= 2007 | volume= 2 | issue= 3 | pages= 418-25 | pmid=17699446 | doi=10.2215/CJN.03361006 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17699446 }} </ref>  Probably the highest recorded incidence came from Hoste et al who studied 5383 ICU patients with a reported rate of AKI of 67% according to the RIFLE criteria (Class R: 12%, Class I: 27%, Class F: 28%).<ref name="pmid16696865">{{cite journal| author=Hoste EA, Clermont G, Kersten A, Venkataraman R, Angus DC, De Bacquer D et al.| title=RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. | journal=Crit Care | year= 2006 | volume= 10 | issue= 3 | pages= R73 | pmid=16696865 | doi=10.1186/cc4915 | pmc=PMC1550961 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16696865 }} </ref>  None of the studies showed any gender preponderance. Generally, lower incidence rates were seen in patients admitted for elective surgery and higher incidence in patients admitted for sepsis.<ref name="pmid23573420">{{cite journal| author=Case J, Khan S, Khalid R, Khan A| title=Epidemiology of acute kidney injury in the intensive care unit. | journal=Crit Care Res Pract | year= 2013 | volume= 2013 | issue= | pages= 479730 | pmid=23573420 | doi=10.1155/2013/479730 | pmc=PMC3618922 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23573420 }} </ref>
 
==Risk Factors==
Risk assessment is an important step in the prevention of AKI especially when certain risk factors are preventable. Risk assessment includes both patient susceptibilities and exposures. Risk factors identified generally depend on the patient population studied.
* '''''In ICU patients''''', those at the highest risk for developing AKI had one or more of the following risk factors: age more than 65 years, diabetes, presence of infection, acute circulatory or respiratory failure, past history of chronic heart failure (CHF), pre-existing kidney disease, lymphoma or leukemia, use of aminoglycosides, or cirrhosis.<ref name="doi10.1007/s001340051281">{{cite journal| author=de Mendonça A, Vincent J, Suter PM, Moreno R, Dearden NM, Antonelli M, Takala J, Sprung C, Cantraine F|title=Acute renal failure in the ICU: risk factors and outcome evaluated by the SOFA score | journal=Intensive Care Medicine | year= 2007 | volume= 26 | issue= 7 | pages= 915-21 | PMID= |doi=10.1007/s001340051281 | pmc= | url=http://link.springer.com/article/10.1007/s001340051281 }} </ref><ref name="pmid16106006">{{cite journal| author=Uchino S, Kellum JA, Bellomo R, Doig GS, Morimatsu H, Morgera S et al.| title=Acute renal failure in critically ill patients: a multinational, multicenter study. | journal=JAMA | year= 2005 | volume= 294 | issue= 7 | pages= 813-8 | pmid=16106006 | doi=10.1001/jama.294.7.813 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16106006 }} </ref><ref name="pmid17728549">{{cite journal| author=Mennel S, Barbazetto I, Meyer CH, Peter S, Stur M| title=Ocular photodynamic therapy--standard applications and new indications. Part 2. Review of the literature and personal experience. | journal=Ophthalmologica | year= 2007 | volume= 221 | issue= 5 | pages= 282-91 |pmid=17728549 | doi=10.1159/000104757 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17728549 }} </ref>
 
* '''''In patients undergoing open heart surgery''''', major risk factors predisposing to postoperative AKI are advanced age, diabetes mellitus, hypertension, impaired left ventricular function, urgent operation or reoperation, prolonged cardiopulmonary bypass and aortic cross-clamp periods, hypothermia, re-exploration for bleeding or pericardial tamponade, systemic infection, peripheral vascular disease, cerebral vascular disease and COPD. CABG was associated with a higher risk for AKI than valve replacement surgery.<ref name="pmid15563569">{{cite journal| author=Thakar CV, Arrigain S, Worley S, Yared JP, Paganini EP| title=A clinical score to predict acute renal failure after cardiac surgery. | journal=J Am Soc Nephrol | year= 2005 | volume= 16 | issue= 1 | pages= 162-8 | pmid=15563569 | doi=10.1681/ASN.2004040331 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15563569 }} </ref><ref name="pmid16363316">{{cite journal| author=Bahar I, Akgul A, Ozatik MA, Vural KM, Demirbag AE, Boran M et al.| title=Acute renal failure following open heart surgery: risk factors and prognosis. | journal=Perfusion | year= 2005 | volume= 20 | issue= 6 | pages= 317-22 | pmid=16363316 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16363316 }} </ref>
 
* '''''In patients exposed to contrast media''''' especially in the context of coronary interventions, pre-existing renal disease is the most important risk factor for contrast induced-AKI (CIAKI). For that, it is indicated to carefully monitor the serum creatinine and GFR before and after PCI. Still, studies have not shown a clear GFR value below which risk of AKI increases drastically. Other important risk factors include, diabetes, hypertension, CHF, advanced age (especially >75), volume depletion, IABP, anemia, hemodynamic instability, concurrent nephrotoxic medications, and high osmolality or large volume of contrast media.<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>
 
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center" width="700px"
|+ '''''Exposures and susceptibilities for non-specific AKI. Adapted from the 2012 KDIGO AKI Practice Guidelines.<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>'''''
| bgcolor="#d9ff54"|'''Exposures''' || bgcolor="#d9ff54"|'''Susceptibilities'''
|-
| Sepsis || Dehydration or volume depletion
|-
| Critical illness || Advanced age
|-
| Circulatory shock || Female gender
|-
| Burns || Black race
|-
| Trauma || CKD
|-
| Cardiac surgery (especially with cardiopulmonary bypass) || Chronic diseases (heart, lung, liver)
|-
| Major non-cardiac surgery || Diabetes mellitus
|-
| Nephrotoxic drugs || Cancer
|-
| Radiocontrast agents || Anemia
|-
| Poisonous plants and animals ||
|}
 
==Differential Diagnosis==
Once acute kidney injury is identified, a large differential diagnosis arises to determine the underlying etiology. A possible differential according to type of AKI is listed below:
 
'''Prerenal AKI:'''
* Congestive heart failure
* Cardiac tamponade
* Cirrhosis
* Nephrotic syndrome
* Hemorrhage
* Dehydration
* Vomiting
* Diarrhea
* Pancreatitis
* NG tube suctionning
* Diuretic overuse
* ACE inhibitor use
* NSAID use
* Renal artery stenosis
* Renal vein thrombosis
* Sepsis
* Vasodilatory drugs
* Anesthesia
 
 
'''Intrinsic renal AKI:'''
* Ischemia - Acute tubular necrosis
* Contrast induced acute kidney injury (CIAKI)
* Thrombotic thrombocytopenic purpura (TTP)
* Hemolytic uremic syndrome (HUS)
* Disseminated intravascular coagulopathy (DIC)
* Acute interstitial nephritis
* Drug toxicity
* Lupus nephropathy
* Henoch-Schonlein purpura (HSP)
* Wegener's granulomatosis
* Goodpasture's syndrome
* Rapidly progressive glomerulonephritis
 
 
'''Postrenal AKI'''
* Bladder neck obstruction
* Bilateral ureteropelvic obstruction
* Nephrolithiasis
* Acute prostatitis
 
[[Image:Algorithm_AKI_diagnosis.jpg|center|600px|Proposed algorithm for the diagnosis of AKI. 2012 KDIGO AKI Practice Guidelines.]]
 
==Natural History, Complications & Prognosis==
The outcomes of AKI vary greatly based on the population studied, the etiology of AKI, and the supportive therapy used. Certain forms of AKI such as contrast induced nephropathy, usually have a shorter course with creatinine peak in 3-5 days and resolution within 1-2 weeks.<ref name="pmid7731155">{{cite journal| author=Rudnick MR, Goldfarb S, Wexler L, Ludbrook PA, Murphy MJ, Halpern EF et al.| title=Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: a randomized trial. The Iohexol Cooperative Study. | journal=Kidney Int | year= 1995 | volume= 47 | issue= 1 | pages= 254-61 | pmid=7731155 | doi= | pmc=|url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7731155 }} </ref>  Acute interstitial nephritis causing AKI can have a variable course, sometimes resolving with the withdrawal of the inciting agent and at times requiring several weeks to restore full renal function. Other forms related to a more severe systemic illness such as DIC, lupus, and RPGN often result in end-stage renal disease. In general, the majority of patients that survive the initial insult recover their kidney function within 30 days.<ref name="doi10.3109/08860228109076011">{{cite journal| author=Kjellstrand CM, Gornick C, Davin T| title=Recovery from Acute Renal Failure | journal=Renal Failure | year=1981 | volume=5 | issue= 1 | pages= 143-61 | pmid= | doi=10.3109/08860228109076011 | pmc= | url=http://informahealthcare.com/doi/abs/10.3109/08860228109076011 }}</ref>  Beyond two months, patients usually will not recover their full renal function but might have some improvement that allows them to be free of renal replacement therapy. The latter represents a very small proportion of patients, particularly elderly patients, and patients with pre-existing CKD. <ref name="pmid17077684">{{cite journal| author=Bagshaw SM| title=Epidemiology of renal recovery after acute renal failure. | journal=Curr Opin Crit Care | year= 2006 | volume= 12 | issue= 6 | pages= 544-50 | pmid=17077684 | doi=10.1097/01.ccx.0000247444.63758.0b | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17077684 }} </ref>
 
 
However, despite the natural history showing possible recovery of renal function, AKI is associated with high mortality. In general, mortality in AKI is highly correlated with the 3 AKI stages, with higher stages increasing the risk of death. In a population based study by Ali et al, 6-month mortality after AKI was 46% in RIFLE stage R, 48% in stage I, and 56 in stage F.<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> In hospitalized patients mortality after AKI ranged from 8.8%<ref name="pmid16696865">{{cite journal| author=Hoste EA, Clermont G, Kersten A, Venkataraman R, Angus DC, De Bacquer D et al.| title=RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. | journal=Crit Care | year= 2006 | volume= 10 | issue= 3 | pages= R73 | pmid=16696865 |doi=10.1186/cc4915 | pmc=PMC1550961 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16696865 }} </ref> to 29.2%<ref name="pmid19547955‎">{{cite journal| author=Joannidis M, Metnitz B, Bauer P, Schusterschitz N, Moreno R, Druml W et al.| title=Acute kidney injury in critically ill patients classified by AKIN versus RIFLE using the SAPS 3 database. | journal=Intensive Care Med | year= 2009 | volume= 35 | issue= 10 | pages= 1692-702 | pmid=19547955‎ | doi=10.1007/s00134-009-1530-4 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19547955 }} </ref> in stage R and from 26.3%<ref name="pmid16696865">{{cite journal| author=Hoste EA, Clermont G, Kersten A, Venkataraman R, Angus DC, De Bacquer D et al.| title=RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. | journal=Crit Care | year= 2006 | volume= 10 | issue= 3 |pages= R73 | pmid=16696865 |doi=10.1186/cc4915 | pmc=PMC1550961 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16696865 }} </ref> to 66.7%<ref name="pmid20714143">{{cite journal| author=Fang Y, Ding X, Zhong Y, Zou J, Teng J, Tang Y et al.| title=Acute kidney injury in a Chinese hospitalized population. | journal=Blood Purif | year= 2010 | volume= 30 | issue= 2 | pages= 120-6 | pmid=20714143 | doi=10.1159/000319972 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20714143 }} </ref> in stage F. Probably the most studied cause of AKI, contrast nephropathy, has given a lot of insight on the mortality with AKI. Levy et al showed that the mortality rate in patients undergoing contrast procedures was 5 fold higher if their post-procedural course was complicated by AKI.<ref name="pmid8622223‎">{{cite journal| author=Levy EM, Viscoli CM, Horwitz RI| title=The effect of acute renal failure on mortality. A cohort analysis. | journal=JAMA | year= 1996 | volume= 275 | issue= 19 | pages= 1489-94 | pmid=8622223‎ | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8622223 }} </ref>
 
Studies have substantiated the association of AKI with poor prognosis not only in terms of mortality. A meta-analysis of studies with long-term AKI follow up showed independent association of AKI with cardiovascular events including MI and stroke. AKI is also associated with ESRD especially in patients with higher stages requiring hemodialysis. The Acute Renal Failure Trials Network (ATN) study showed that patients on hemodilysis after AKI had only a 50% chance of recovering their kidney function after 28 days.
 
AKI is also associated with increased length of hospital stay and costs. A study by Ishani et al showed that small increases in serum creatinine (≥0.5 mg/dl) were associated with a 6.5-fold higher mortality, a 3.5 day increase in length of stay, and around $7500 in added costs.


==Diagnosis==
==Diagnosis==
===Signs and Symptoms===
[[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]]
Signs and symptoms of AKI are limited and often unrecognized early on. The major clinical symptoms include decreased urine output and dark colored urine. Other symptoms are largely non-specific and related to azotemia. Patients may complain of malaise, nausea, pruritis, confusion, and a metallic taste. History should focus on determining the possible etiologies. History of volume depletion secondary to vomiting, diarrhea, or diuretics use should point to a pre-renal cause of AKI. Medications should be noted carefully for the intake of NSAIDs, ACE inhibitors, ARBs, and other medications with known nephrotoxic properties. A history of prostatic hypertrophy or cancer, nephrolithiasis, or malignancy could be a sign of post-renal obstruction.
 
Signs on physical exam may show volume overload, orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes with asterixis and a friction rub occasionally present in late disease. <ref name="pmid13489601">{{cite journal| author=PALMER RA, HENRY EW| title=The clinical course of acute renal failure; observations on 54 cases. | journal=Can Med Assoc J | year= 1957 | volume= 77 | issue= 12 | pages= 1078-84 | pmid=13489601 | doi= | pmc=PMC1824321 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13489601 }} </ref>
 
===Lab Findings===
Clinical signs of AKI are scarce prompting aggressive laboratory surveillance especially in high-risk patients. With past diagnostic strategies, the diagnosis of AKI depended on an elevation of BUN and serum creatinine without response to a fluid challenge. However, this approach alone is not enough. Proper diagnosis and management on AKI requires careful examination of serum chemistries, urinary chemistries and sediments.<ref name="pmid15232604">{{cite journal| author=Schrier RW, Wang W, Poole B, Mitra A| title=Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. | journal=J Clin Invest | year= 2004 | volume= 114 | issue= 1 | pages= 5-14 | pmid=15232604 | doi=10.1172/JCI22353 | pmc=PMC437979 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15232604 }} </ref>
 
Diagnosis of AKI is usually made by documenting an acute elevation in BUN and serum creatinine. Serum creatinine is also used to monitor disease progression and may hint to the etiology of the acute insult. For example, prerenal azotemia usually causes a small increase in serum creatinine that returns to baseline with the improvement of hemodynamics while contrast-induced nephropathy usually causes a rise in serum creatinine 24–48 hours after exposure, peaking within 3 to 5 days, and resolving within 1 week.
 
AKI may also lead to severe electrolyte disturbances such as hyperkalemia, hyperphosphatemia, and hypocalcemia that need regular follow-up and may often need corrective measures. Other findings may also help detect the etiology of AKI and are disease specific.<ref name="pmid23402809">{{cite journal| author=Combadière C, Raoul W, Guillonneau X, Sennlaub F| title=Comment on "Ccl2, Cx3cr1 and Ccl2/Cx3cr1 chemokine deficiencies are not sufficient to cause age-related retinal degeneration" by Luhmann et al. (Exp. Eye Res. 2013; 107: 80.doi: 10.1016). | journal=Exp Eye Res | year= 2013 | volume= 111 | issue= | pages= 134-5 | pmid=23402809 | doi=10.1016/j.exer.2013.02.002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23402809 }} </ref>
 
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center"
|+ '''''Disease specific blood laboratory findings'''''
| bgcolor="#d9ff54"|'''Blood Laboratory Finding''' || bgcolor="#d9ff54"|'''Related Etiologies'''
|-
| bgcolor="#ececec"|'''Severe hyperphosphatemia, hypocalcemia, elevated CPK and uric acid''' || Tumor Lysis Syndrome, Rhabdomyolysis
|-
| bgcolor="#ececec"|'''Increased anion gap and osmolal gap''' || Ethylene Glycol Poisoning
|-
| bgcolor="#ececec"|'''Low anion gap''' || Multiple Myeloma
|-
| bgcolor="#ececec"|'''Low complement levels and high titers of ANAs, ANCAs and cryoglobulins''' || Vasculitides
|-
| bgcolor="#ececec"|'''Severe anemia in the absence of bleeding''' || Hemolysis, Multiple Myeloma
 
|-
| bgcolor="#ececec"|'''Anemia, thrombocytopenia, schistocytes on peripheral blood smear, elevated LDH, and low haptoglobin''' || TTP, HUS, DIC
 
|-
| bgcolor="#ececec"|'''Peripheral eosinophilia''' || Acute interstitial nephritis, atheroembolic disease, polyarteritis nodosa, Churg-Strauss
|-
| bgcolor="#ececec"|'''Elevated BNP''' || Heart Failure
 
|-
| bgcolor="#ececec"|'''Bacteremia''' || Sepsis
 
|}
 
 
Urine is a very important marker of kidney function and injury, and a urinalysis is almost invariably a crucial tool for the detection of the etiology and site of injury in AKI. AKI may be defined by oliguria alone; however, urine output is not necessarily decreased. Urine should be noted for volume, color, specific gravity, proteinuria, hematuria, pyuria, and sodium and creatinine concentrations.
 
Careful urine sediment examination is essential and may show hyaline casts, granular casts, red blood cells casts and tubular epithelial cell casts each denoting a different site and etiology for the AKI For instance, RBC casts in the urine sediment strongly suggest a glomerular or vascular cause of AKI. Acute tubular necrosis secondary to ischemia classically gives muddy-brown casts, pigmented granular casts, and epithelial cell casts. Tumor lysis syndrome would show uric acid crystals in the urine. Still, it is important to correlate the urinary sediment examination to the clinical context since urinary sediment findings have a low specificity when used alone.<ref name="pmid18953176">{{cite journal| author=Chawla LS, Dommu A, Berger A, Shih S, Patel SS| title=Urinary sediment cast scoring index for acute kidney injury: a pilot study. | journal=Nephron Clin Pract | year= 2008 | volume= 110 | issue= 3 | pages= c145-50 | pmid=18953176 | doi=10.1159/000166605 | pmc=PMC2605880 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18953176 }} </ref>
 
Several calculated indices can also be used in the diagnosis of AKI including BUN/creatinine ratio, fractional excretion of sodium & fractional excretion of urea. In prerenal azotemia, low tubular flow rate and enhanced recycling of urea causes an uneven elevation in the BUN compared to creatinine which may manifest as an elevated BUN/creatinine ratio (greater than 20:1). In intrinsic renal AKI however, urea reabsorption is not elevated, so BUN and serum creatinine concentrations increase proportionally usually preserving the BUN/creatinine ratio (10-20:1).<ref name="pmid23402809">{{cite journal| author=Combadière C, Raoul W, Guillonneau X, Sennlaub F| title=Comment on "Ccl2, Cx3cr1 and Ccl2/Cx3cr1 chemokine deficiencies are not sufficient to cause age-related retinal degeneration" by Luhmann et al. (Exp. Eye Res. 2013; 107: 80.doi: 10.1016). | journal=Exp Eye Res | year= 2013 | volume= 111 | issue= | pages= 134-5 | pmid=23402809 | doi=10.1016/j.exer.2013.02.002 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23402809 }} </ref>
 
Another important index used in AKI is the fractional excretion of sodium (FE<sub>Na</sub>). The FE<sub>Na</sub> represents the fraction of filtered sodium load that is excreted in the urine and is a measure of tubular function by the kidney's ability to reabsorb sodium. The FE<sub>Na</sub> is calculated by the following equation:
 
[[Image:FEna.png|center]]
 
 
In prerenal azotemia, tubular function is preserved and sodium reabsorption increases with the associated renal vasoconstriction. Hence the FE<sub>Na</sub> is usually <1% in prerenal azotemia. A high FE<sub>Na</sub> in the context of prerenal azotemia is possible during diuretic treatment and glycosuria.
 
Another important index is the fractional excretion of urea (FE<sub>urea</sub>) calculated using the same equation for the fractional excretion of sodium. FE<sub>urea</sub> is of value in states of reduced effective circulating volume, and in cases where diuretics have been administered. In these situations, a low FEurea (<35%) has a higher sensitivity and specificity than FE<sub>Na</sub> in differentiating between prerenal azotemia and renal AKI.<ref name="pmid12427149">{{cite journal| author=Carvounis CP, Nisar S, Guro-Razuman S| title=Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. | journal=Kidney Int | year= 2002 | volume= 62 | issue= 6 | pages= 2223-9 | pmid=12427149 | doi=10.1046/j.1523-1755.2002.00683.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12427149 }} </ref>
 
 
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
|+ '''''Distinguishing Prerenal azotemia and ATN'''''
| bgcolor="#d9ff54"|'''Parameter''' || bgcolor="#d9ff54"|'''Prerenal AKI''' || bgcolor="#d9ff54"|'''Acute Tubular Necrosis'''
|-
| bgcolor="#ececec"|'''Urinary sediment''' || Normal/Hyaline casts || Epithelial cell casts
|-
| bgcolor="#ececec"|'''Urine specific gravity''' || >1.020 || <1.020
|-
| bgcolor="#ececec"|'''Urine sodium (mmol/L)''' || <20 || >40
|-
| bgcolor="#ececec"|'''FE<sub>Na</sub>''' || <1% || >2%
|-
| bgcolor="#ececec"|'''FE<sub>urea</sub>''' || <35% || >50%
|-
| bgcolor="#ececec"|'''Urine osmolality (mOsmol/kg H<sub>2</sub>O)''' || >500 || <350
|-
| bgcolor="#ececec"|'''Urine-Plasma creatinine ratio''' || >40 || <10
|-
| bgcolor="#ececec"|'''Plasma BUN-creatinine ratio''' || >20 || <15
|}
 
===Novel Biomarkers===
Serum creatinine has been criticized as a means to define AKI due to its lack of accuracy especially since creatinine secretion is increased with a decreasing GFR, leading to a less obvious rise in serum creatinine.<ref name="pmid11505124">{{cite journal| author=Erley CM, Bader BD, Berger ED, Vochazer A, Jorzik JJ, Dietz K et al.| title=Plasma clearance of iodine contrast media as a measure of glomerular filtration rate in critically ill patients. | journal=Crit Care Med | year= 2001 | volume= 29 | issue= 8 | pages= 1544-50 | pmid=11505124 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11505124 }} </ref>  Creatinine excretion is then considerably greater than the filtered load, leading to an overestimation of the GFR.<ref name="pmid13887292">{{cite journal| author=DOOLAN PD, ALPEN EL, THEIL GB| title=A clinical appraisal of the plasma concentration and endogenous clearance of creatinine. | journal=Am J Med | year= 1962 | volume= 32 | issue= | pages= 65-79 | pmid=13887292 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13887292 }} </ref>  Furthermore, serum creatinine and BUN are both measures of renal filtration and are thus not direct markers of parenchymal injury. Creatinine is a poor marker of very early kidney injury, and is seldom used to predict and prevent the occurrence of AKI.
 
Novel biomarkers have been implicated in the diagnosis and early detection of AKI. Markers such as Kidney injury molecule-1 (KIM-1), Neutrophil gelatinase associated lipocalin (NGAL), and Cystatin C among others have shown great promise in recent trials. However, the availability, low cost, and ease of measuring serum creatinine and the ability to monitor the progression of the disease with serial measurements still make creatinine a biomarker of choice in AKI for a majority of centers.<ref name="pmid21493774">{{cite journal| author=Siew ED, Ware LB, Ikizler TA| title=Biological markers of acute kidney injury. | journal=J Am Soc Nephrol | year= 2011 | volume= 22 | issue= 5 | pages= 810-20 | pmid=21493774 | doi=10.1681/ASN.2010080796 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21493774 }} </ref>
 
{| border="1" style="border-collapse:collapse; text-align:center;" cellpadding="5" align="center"
|+ '''''Novel biomarkers of AKI. Modified from Siew, Ware, & Ikizler (2011)<ref name="pmid21493774">{{cite journal| author=Siew ED, Ware LB, Ikizler TA| title=Biological markers of acute kidney injury. | journal=J Am Soc Nephrol | year= 2011 | volume= 22 | issue= 5 | pages= 810-20 | pmid=21493774 | doi=10.1681/ASN.2010080796 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21493774 }} </ref>'''''
| bgcolor="#d9ff54"|'''Biomarker''' || bgcolor="#d9ff54"|'''Source''' || bgcolor="#d9ff54"|'''Site of Expression'''||bgcolor="#d9ff54"|'''Biomarker Property'''
|-
| bgcolor="#ececec"|'''NGAL''' || Urine and Serum || Proximal tubule > Distal tubule || Upregulated expression during ischemic injury and detectable in urine
|-
| bgcolor="#ececec"|'''KIM-1''' || Urine || Proximal tubule || Ectodomain shed into urine following injury
|-
| bgcolor="#ececec"|'''Cystatin C''' || Urine and Serum || Nucleated cells || Accumulates in serum as filtration decreases due to impaired proximal tubule metabolism
|-
| bgcolor="#ececec"|'''NAG''' || Urine || Proximal tubule || Lysosomal enzyme in proximal tubule
|-
| bgcolor="#ececec"|'''L-FABP''' || Urine || Proximal tubule, liver, small intestine || Translocation from cytosol to tubular lumen during ischemic injury
|-
| bgcolor="#ececec"|'''NHE-3''' || Urine || Proximal tubule and Thick ascending loop || Most abundant sodium transporter in proximal tubule lost in urine during injury
|-
| bgcolor="#ececec"|'''Netrin-1''' || Urine ||Proximal tubule blood vessels, lung, pancreas, mammary gland ||  Increased expression early after ischemia-reperfusion and nephrotoxin injury
 
|}


==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===
===Prophylaxis===
===Future or Investigational Therapies===
 
==AKI and Chronic Kidney Disease==
 
==See also==
* [[BUN-to-creatinine ratio]]
* [[Chronic kidney disease]]
* [[Dialysis]]
* [[Renal failure]]
* [[Rhabdomyolysis]]
* [[Contrast-induced nephropathy]]


==Related Chapters==
==Case Studies==
*[[Chronic renal failure|Chronic Renal Failure]]
[[Acute kidney injury case study one|Case #1]]
*[[Dialysis]]
*[[Hepatorenal syndrome|Hepatorenal Syndrome]]
*[[Renal failure|Renal Failure]]


==References==
{{Reflist|2}}
{{Nephrology}}
{{Nephrology}}
{{Organ failure}}
{{Organ failure}}


[[Category:Causes of death]]
 
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]
[[Category:Kidney diseases]]
[[Category:Medical emergencies]]
[[Category:Medicine]]
[[Category:Medicine]]
[[Category:Nephrology]]
[[Category:Nephrology]]
[[Category:Organ failure]]
[[Category:Up-To-Date]]


{{WH}}
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Latest revision as of 20:20, 31 July 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Serge Korjian M.D., Farima Kahe M.D. [2]

Synonyms and keywords: Acute kidney failure; acute renal failure; acute uremia; AKI; ARF; uremia,

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