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| __NOTOC__
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| {{CMG}}
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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 2004, 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.
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| |+ RIFLE criteria to define acute kidney injury (AKI)
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| | bgcolor="#d9ff54"|Classification || U<sub>Osm</sub> || U<sub>Na</sub> || Fe<sub>Na</sub> || [[BUN-to-creatinine ratio|BUN/Cr]]
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| | bgcolor="#d9ff54"|Prerenal || >500 || <10 || <1% || >20 | | | {{#ev:youtube|https://https://www.youtube.com/watch?v=vnTR_y3Sf-k|350}} |
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| | Intrinsic || <350 || >20 || >2% || <15{{cn|date=November 2012}}
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| | Postrenal || <350 || >40 || >4% || >15
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| In 2007, the Acute Kidney Injury Network (AKIN) proposed a modified diagnostic criteria based on the RIFLE criteria. AKI was defined as an acute increase in the serum creatinine of ≥0.3 mg/dL from baseline within 48 hours, a 50% increase in the serum creatinine concentration, or oliguria <0.5 mL/kg/h for 6 hours (following volume status optimization). The staging criteria retained the Risk, Injury, & Failure stages from the RIFLE criteria, with modifications related to serum creatinine increase.
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| {| class="wikitable" style="float:right; text-align:center" | |
| |+ Classic laboratory findings in AKI
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| ! Type !! U<sub>Osm</sub> !! U<sub>Na</sub> !! Fe<sub>Na</sub> !! [[BUN-to-creatinine ratio|BUN/Cr]]
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| | Prerenal || >500 || <10 || <1% || >20
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| | Intrinsic || <350 || >20 || >2% || <15{{cn|date=November 2012}}
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| | Postrenal || <350 || >40 || >4% || >15 | | | [[File:Siren.gif|link=Acute kidney failure resident survival guide|41x41px]]|| <br> || <br> |
| | | [[Acute kidney failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| |} | | |} |
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| In March 2012, the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for Acute Kidney Injury retained the AKIN staging criteria while implementing modifications to the definition of AKI. They developed definition and staging criteria for AKI that combined previous definitions into a more clinically applicable one. AKI was defined as either:
| | {{Acute kidney injury}} |
| | | {{CMG}} {{AE}} {{SSK}}, {{F.K}} |
| * 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
| | {{SK}} Acute kidney failure; acute renal failure; acute uremia; AKI; ARF; uremia, |
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| ==Historical Perspective== | | ==[[Acute kidney injury overview|Overview]]== |
| 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.
| | ==[[Acute kidney injury historical perspective|Historical Perspective]]== |
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| ==Classification== | | ==[[Acute kidney injury classification|Classification]]== |
| Acute kidney injury is diagnosed on the basis of [[clinical history]] and laboratory data. A diagnosis is made when there is rapid reduction in [[renal function|kidney function]], as measured by serum [[creatinine]], or based on a rapid reduction in urine output, termed [[oliguria]]. | |
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| ===Definition=== | | ==[[Acute kidney injury pathophysiology|Pathophysiology]]== |
| Introduced by the [[Acute Kidney Injury Network]] (AKIN), specific criteria exist for the diagnosis of AKI:<ref name="pmid17331245">{{cite journal |author=Mehta RL, Kellum JA, Shah SV, ''et al.'' |title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury |journal=Critical Care (London, England) |volume=11 |issue=2 |pages=R31 |year=2007 |pmid=17331245 |pmc=2206446 |doi=10.1186/cc5713 |url=http://ccforum.com/content/11/2/R31}}</ref>
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| # Rapid time course (less than 48 hours)
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| # Reduction of kidney function
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| #* Rise in serum [[creatinine]], defined by either:
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| #** Absolute increase in serum creatinine of ≥0.3 mg/dl (≥26.4 μmol/l)
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| #** Percentage increase in serum creatinine of ≥50%
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| #* Reduction in urine output, defined as <0.5 ml/kg/hr for more than 6 hours
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| ===Staging=== | | ==[[Acute kidney injury causes|Causes]]== |
| The ''RIFLE criteria'', proposed by the [[Acute Dialysis Quality Initiative]] (ADQI) group, aid in the staging of patients with AKI:<ref>{{cite journal |author=Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P |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 |volume=8 |issue=4 |pages=R204–12 |year=2004 |pmid=15312219 |pmc=522841 |doi=10.1186/cc2872 |url=http://ccforum.com/content/8/4/R204}}</ref><ref>{{cite journal |author=Lameire N, Van Biesen W, Vanholder R |title=Acute renal failure |journal=[[The Lancet|Lancet]] |volume=365 |issue=9457 |pages=417–30 |year=2005 |pmid=15680458 |doi=10.1016/S0140-6736(05)17831-3}}</ref>
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| * Risk: GFR decrease >25%, serum creatinine increased 1.5 times or urine production of <0.5 ml/kg/hr for 6 hours
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| * Injury: GFR decrease >50%, doubling of creatinine or urine production <0.5 ml/kg/hr for 12 hours
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| * Failure: GFR decrease >75%, tripling of creatinine or creatinine >355 μmol/l (with a rise of >44) (>4 mg/dl) OR urine output below 0.3 ml/kg/hr for 24 hours
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| * Loss: persistent AKI or complete loss of [[renal function|kidney function]] for more than 4 weeks
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| * [[End-stage renal disease]]: need for renal replacement therapy (RRT) for more than 3 months
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| ==Pathophysiology== | | ==[[Acute kidney injury differential diagnosis|Differentiating Acute kidney injury from other Diseases]]== |
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| ==Causes== | | ==[[Acute kidney injury epidemiology and demographics|Epidemiology and Demographics]]== |
| AKI can be caused by disease, [[crush syndrome|crush injury]], [[Contrast-induced nephropathy|contrast agents]], some antibiotics, and more.
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| The causes of acute kidney injury are commonly categorized into ''prerenal'', ''intrinsic'', and ''postrenal''.
| | ==[[Acute kidney injury risk factors|Risk Factors]]== |
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| {| class="wikitable" style="float:right; text-align:center"
| | ==[[Acute kidney injury screening|Screening]]== |
| |+ Classic laboratory findings in AKI
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| ! Type !! U<sub>Osm</sub> !! U<sub>Na</sub> !! Fe<sub>Na</sub> !! [[BUN-to-creatinine ratio|BUN/Cr]]
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| | Prerenal || >500 || <10 || <1% || >20
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| | Intrinsic || <350 || >20 || >2% || <15{{cn|date=November 2012}}
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| | Postrenal || <350 || >40 || >4% || >15
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| |}
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| ===Prerenal=== | | ==[[Acute kidney injury natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| ''Prerenal'' causes of AKI ("pre-renal azotemia") are those that decrease effective [[renal blood flow|blood flow to the kidney]]. These include systemic causes, such as [[hypovolemia|low blood volume]], [[hypotension|low blood pressure]], [[heart failure]], and local changes to the blood vessels supplying the kidney. The latter include [[renal artery stenosis]], or the narrowing of the [[renal artery]] which supplies the kidney with blood, and [[renal vein thrombosis]], which is the formation of a [[thrombus|blood clot]] in the [[renal vein]] that drains blood from the kidney.
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| [[Renal ischaemia]] ultimately results in functional disorder, depression of [[Glomerular filtration rate|GFR]], or both. These causes stem from the inadequate cardiac output and hypovolemia or vascular diseases causing reduced perfusion of both kidneys. Both kidneys need to be affected as one kidney is still more than adequate for normal kidney function.
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| ===Intrinsic===
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| Sources of damage to the kidney itself are dubbed ''intrinsic''. Intrinsic AKI can be due to damage to the [[glomerulus (kidney)|glomeruli]], [[nephron|renal tubules]], or [[interstitium]]. Common causes of each are [[glomerulonephritis]], [[acute tubular necrosis]] (ATN), and [[acute interstitial nephritis]] (AIN), respectively. A cause of intrinsic acute renal failure is [[tumor lysis syndrome]].<ref>{{cite book|last=Jim Cassidy, Donald Bissett, Roy A. J. Spence, Miranda Payne|first=|title=Oxford Handbook of Oncology |url=http://books.google.com/books?id=WKoQW4G0g14C&pg=PA706&dq=tumour+lysis+syndrome+acute+renal+failure&hl=en&sa=X&ei=lbigT8KJPMeEgwehjfWmCQ&ved=0CFYQ6AEwBQ#v=onepage&q=tumour%20lysis%20syndrome%20acute%20renal%20failure&f=false|date=1 January 2010|publisher=[[Oxford University Press]]|page=706}}</ref>
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| ===Postrenal===
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| ''Postrenal'' AKI is a consequence of [[urinary tract]] obstruction. This may be related to [[benign prostatic hyperplasia]], [[kidney stone]]s, obstructed [[urinary catheter]], bladder stone, bladder, ureteral or renal malignancy. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted immediately after urinating to measure fluid still in the bladder. 50-100ml suggests neurogenic bladder. A renal ultrasound will demonstrate hydronephrosis if present. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis, however, in case of acute renal failure, the use of IV contrast is contraindicated. On the basic metabolic panel, the [[BUN-to-creatinine ratio|ratio of BUN to creatinine]] may indicate post renal failure.
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| ==Epidemiology==
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| New cases of AKI are unusual but not rare, affecting approximately 0.1% of the UK population per year (2000 ppm/year), 20x incidence of new ESRD. AKI requiring dialysis (10% of these) is rare (200 ppm/year), 2x incidence of new ESRD.<ref>{{cite web|url=http://www.renalmed.co.uk/database/acute-kidney-injury-aki |title=Renal Medicine: Acute Kidney Injury (AKI) |publisher=Renalmed.co.uk |date=2012-05-23 |accessdate=2013-07-17}}</ref>
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| Acute kidney injury is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the [[intensive care unit]].<ref name="isbn1-4160-3110-3">{{cite book |author= |title=Brenner and Rector's The Kidney |publisher=Saunders |location=Philadelphia |year=2007 |pages= |isbn=1-4160-3110-3 |oclc= |doi= |accessdate=}}</ref> | |
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| ==Risk Factors==
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| ==Natural History==
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| ==Complications==
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| [[Metabolic acidosis]], [[hyperkalemia]], and [[pulmonary edema]] may require medical treatment with [[sodium bicarbonate]], antihyperkalemic measures, and diuretics.
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| Lack of improvement with [[Fluid replacement|fluid resuscitation]], therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate [[renal replacement therapy|artificial support]] in the form of [[dialysis]] or [[hemofiltration]].<ref name=Weisberg/>
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| ==Prognosis==
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| Depending on the cause, a proportion of patients will never regain full renal function, thus entering [[end-stage renal failure]] and requiring lifelong dialysis or a [[kidney transplant]]. Patients with AKI are more likely to die prematurely after they were discharged from hospital even if their kidney function has recovered.<ref name=harrison18 />
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| ==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]] |
| The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as [[fatigue (medical)|fatigue]], [[Anorexia (symptom)|loss of appetite]], [[headache]], [[nausea]] and [[vomiting]].<ref name=Skorecki>{{cite book |author=Skorecki K, Green J, Brenner BM |editor=Kasper DL, Braunwald E, Fauci AS, ''et al.'' |title=Harrison's Principles of Internal Medicine|edition=16th |year=2005 |publisher=McGraw-Hill |location=New York, NY |isbn=0-07-139140-1 |pages=1653–63 |chapter=Chronic renal failure}}</ref> Marked increases in the [[potassium]] level can lead to [[cardiac arrhythmia|irregularities in the heartbeat]], which can be severe and life-threatening.<ref name=Weisberg>{{cite journal |author=Weisberg LS |title=Management of severe hyperkalemia |journal=Crit. Care Med. |volume=36 |issue=12 |pages=3246–51 |year=2008 |month=December |pmid=18936701 |doi=10.1097/CCM.0b013e31818f222b}}</ref> Fluid [[homeostasis|balance]] is frequently affected, though [[hypertension]] is rare.<ref name=cmdt>{{cite book|last=Tierney|first=Lawrence M. |coauthors=Stephen J. McPhee and Maxine A. Papadakis|title=CURRENT Medical Diagnosis and Treatment 2005|accessdate=2011-08-05|edition=44|year=2004|publisher=[[McGraw-Hill]]|isbn=0-07-143692-8|page=871|chapter=22}}</ref>
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| Pain in the flanks may be encountered in some conditions (such as [[thrombosis]] of the renal blood vessels or inflammation of the kidney); this is the result of stretching of the [[renal capsule|fibrous tissue capsule surrounding the kidney]].<ref name=Brady>{{cite book |author=Brady HR, Brenner BM |editor=Kasper DL, Braunwald E, Fauci AS, ''et al.'' |title=Harrison's Principles of Internal Medicine|edition=16th |year=2005 |publisher=McGraw-Hill |location=New York, NY |isbn=0-07-139140-1 |pages=1644–53 |chapter=Chronic renal failure}}</ref> If the kidney injury is the result of dehydration, there may be [[thirst]] as well as evidence of fluid depletion on [[physical examination]].<ref name=Brady/> Physical examination may also provide other clues as to the underlying cause of the kidney problem, such as a [[rash]] in interstitial nephritis and a palpable [[urinary bladder|bladder]].<ref name=Brady/>
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| Inability to excrete sufficient fluid from the body can cause accumulation of fluid in the limbs ([[peripheral edema]]) and the lungs ([[pulmonary edema]]),<ref name=Skorecki/> as well as [[cardiac tamponade]] as a result of fluid [[effusion]]s.<ref name=cmdt />
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| ===Detection===
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| The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of [[blood test]]s for substances normally eliminated by the kidney: [[urea]] and [[creatinine]]. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as [[NGAL]], [[KIM-1]], [[Interleukin 18|IL18]] and [[cystatin C]]), but none are currently established enough to replace creatinine as a marker of renal function.{{citation needed|date=April 2011}} {{When|date=April 2011}}
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| Sodium and potassium, two electrolytes that are commonly deranged in people with acute kidney injury, are typically measured together with urea and creatinine.{{citation needed | date=April 2011}}
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| ===Further testing===
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| Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. These may include urine sediment analysis, [[renal ultrasound]] and/or [[kidney biopsy]]. Indications for renal biopsy in the setting of AKI include:<ref name="isbn0-07-159124-9">{{cite book |author=Papadakis MA, McPhee SJ |title=Current Medical Diagnosis and Treatment |publisher=McGraw-Hill Professional |location= |year=2008 |pages= |isbn=0-07-159124-9}}</ref>
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| # Unexplained AKI
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| # AKI in the presence of the [[nephritic syndrome]]
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| # Systemic disease associated with AKI
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| ==Treatment== | | ==Treatment== |
| The management of AKI hinges on identification and treatment of the underlying cause. In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called [[nephrotoxin]]s. These include [[NSAID]]s such as [[ibuprofen]], [[iodinated contrast]]s such as those used for [[CT scan]]s, many [[antibiotics]] such as [[gentamicin]], and a range of other substances.<ref name=pmid18492867 />
| | [[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]] |
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| Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a [[urinary catheterization|urinary catheter]] helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.
| | ==Case Studies== |
| | [[Acute kidney injury case study one|Case #1]] |
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| ===Specific therapies===
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| In prerenal AKI without [[hypervolemia|fluid overload]], administration of [[intravenous fluid]]s is typically the first step to improve renal function. Volume status may be monitored with the use of a [[central venous catheter]] to avoid over- or under-replacement of fluid.
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| Should [[hypotension|low blood pressure]] prove a persistent problem in the fluid-replete patient, [[inotrope]]s such as [[norepinephrine]] and [[dobutamine]] may be given to improve [[cardiac output]] and hence renal perfusion. While a useful pressor, there is no evidence to suggest that [[dopamine]] is of any specific benefit,<ref>{{cite journal |author=Holmes CL, Walley KR |title=Bad medicine: low-dose dopamine in the ICU |journal=Chest |volume=123 |issue=4 |pages=1266–75 |year=2003 |pmid=12684320|doi=10.1378/chest.123.4.1266}}</ref> and may be harmful.
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| The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to [[Wegener's granulomatosis]] may respond to [[steroid]] medication. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as [[aminoglycoside]], [[penicillin]], NSAIDs, or [[paracetamol]].<ref name=Brady />
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| If the cause is obstruction of the urinary tract, relief of the obstruction (with a [[nephrostomy]] or [[urinary catheter]]) may be necessary.
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| ===Diuretic agents===
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| The use of [[diuretics]] such as [[furosemide]], is widespread and sometimes convenient in ameliorating fluid overload, and is not associated with higher mortality (risk of death).<ref>{{cite journal |author=Uchino S, Doig GS, Bellomo R, ''et al'' |title=Diuretics and mortality in acute renal failure |journal=Crit. Care Med. |volume=32 |issue=8 |pages=1669–77 |year=2004 |pmid=15286542|doi=10.1097/01.CCM.0000132892.51063.2F}}</ref>
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| ===Renal replacement therapy===
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| [[Renal replacement therapy]], such as with [[hemodialysis]], may be instituted in some cases of AKI. A systematic review of the literature in 2008 demonstrated no difference in outcomes between the use of [[intermittent hemodialysis]] and [[continuous venovenous hemofiltration]] (CVVH).<ref name="pmid18285591">{{cite journal |author=Pannu N, Klarenbach S, Wiebe N, Manns B, Tonelli M |title=Renal replacement therapy in patients with acute renal failure: a systematic review |journal=JAMA : the Journal of the American Medical Association |volume=299 |issue=7 |pages=793–805 |year=2008 |month=February |pmid=18285591 |doi=10.1001/jama.299.7.793 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=18285591}}</ref> Among critically ill patients, intensive renal replacement therapy with CVVH does not appear to improve outcomes compared to less intensive intermittent hemodialysis.<ref name="pmid18492867">{{cite journal |author=Palevsky PM, Zhang JH, O'Connor TZ, ''et al.'' |title=Intensity of renal support in critically ill patients with acute kidney injury |journal=The New England Journal of Medicine |volume=359 |issue=1 |pages=7–20 |year=2008 |month=July |pmid=18492867 |pmc=2574780 |doi=10.1056/NEJMoa0802639 |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=18492867&promo=ONFLNS19}}</ref><ref name="pmid19846848">{{cite journal |author=Bellomo R, Cass A, Cole L, ''et al.'' |title=Intensity of continuous renal-replacement therapy in critically ill patients |journal=The New England Journal of Medicine |volume=361 |issue=17 |pages=1627–38 |year=2009 |month=October |pmid=19846848 |doi=10.1056/NEJMoa0902413 |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=19846848&promo=ONFLNS19}}</ref>
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| ==See also==
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| * [[BUN-to-creatinine ratio]]
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| * [[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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| ==Acute Renal Failure Videos==
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| ===Acute Renal Failure 1===
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| {{#ev:youtube|cPIk7iLMwOI}}
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| ===Acute Renal Failure 2===
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| {{#ev:youtube|MmQKGeAyUOM}}
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| ===Acute Renal Failure 3===
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| {{#ev:youtube|8IU0ABdvCQA}}
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| ===Acute Renal Failure 4===
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| {{#ev:youtube|VxzIE6npBTk}}
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| ===Acute Renal Failure 5===
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| {{#ev:youtube|IyLC9b1Bilc}}
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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}} |
