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Curr Opin Nephrol Hypertens. Author manuscript; available in PMC Jan 26, 2011.
Published in final edited form as:
PMCID: PMC3027554

The incidence and prognostic significance of acute kidney injury


Purpose of review

Acute kidney injury is an increasingly common and potentially catastrophic complication in hospitalized patients. This review summarizes the major epidemiologic studies that have informed our understanding of the incidence and prognostic significance of acute kidney injury.

Recent findings

Early observational studies from the 1980s and 1990s established the general epidemiologic features of acute kidney injury, including the incidence, prognostic significance and predisposing medical and surgical conditions. Recent multicenter observational cohorts and administrative databases have enhanced our understanding of the overall disease burden of acute kidney injury and trends in its epidemiology. An increasing number of clinical studies focusing on specific types of acute kidney injury (e.g. following exposure to intravenous contrast, sepsis and major surgery) have provided further details into this heterogeneous syndrome.


In light of the increasing incidence and prognostic significance of acute kidney injury, new strategies for prevention and treatment are desperately needed.

Keywords: acute kidney injury, acute renal failure, epidemiology, incidence, outcomes


Acute renal failure (ARF), often referred to as ‘acute kidney injury’ (AKI), is characterized by sudden (i.e. hours to days) impairment of kidney function. AKI is now understood to be an increasingly common and potentially catastrophic complication in hospitalized patients. This review summarizes recent epidemiologic studies of AKI, including early observational studies, recent large cohort studies and administrative/claims database investigations.

Early epidemiologic studies of acute kidney injury

The first prospective cohort studies of AKI were performed in individual centers and provided insights into the frequency, causes and prognostic significance of AKI. Hou et al. [1], in 1983, found that 4.9% of hospitalized patients developed AKI [defined as a relative increase in serum creatinine (SCr) of 0.5, 1.0 or 1.5 mg/dl, depending on the baseline SCr]. The major causes of hospital-acquired AKI were decreased renal perfusion (42%), major surgery (18%), contrast nephropathy (12%) and aminoglycoside antibiotics (7%). The crude in-hospital mortality rate was 25% and was higher in those with more significant degrees of AKI.

Nash et al. [2] updated their initial study of hospital-acquired AKI almost two decades later. They reported that 7.2% of patients developed AKI – higher than the 4.9% in the original study performed at a different institution, although the in-hospital mortality rate (19.4%) was slightly lower. The most common causes of AKI in the follow-up study were decreased renal perfusion (39%; defined broadly to include congestive heart failure, cardiac arrest, and volume contraction), nephrotoxin administration (16%), contrast administration (11%) and major surgery (9%).

Multicenter observational cohort studies of acute kidney injury

Regardless of how carefully conducted, single-center studies are inherently limited in terms of sample size and external validity (i.e. generalizability to AKI at other medical centers). Recognizing this limitation, investigators have launched multicenter epidemiologic investigations of AKI.

The first multicenter observational studies of AKI were published in the mid-1990s by Liano et al. [3] and Brivet et al. [4]. Results from the two most recent multicenter studies are described below.

The Program to Improve Care in Acute Renal Disease (PICARD) investigators [5] performed a 31-month-long, prospective observational cohort study of patients at five academic medical centers in the United States from 1999 to 2001. Eligible patients were those in the intensive care unit for whom nephrologic consultation was obtained; AKI was defined as an increase in SCr of at least 0.5 mg/dl if baseline was less than or equal to 1.5 mg/dl, or an increase of at least 1.0 mg/dl if baseline SCr was between 1.6 and 4.9 mg/dl.

A total of 618 patients were enrolled in PICARD. One of the most illustrative findings in PICARD was the degree of heterogeneity of patients with AKI across the five medical centers in terms of baseline characteristics, processes of care and in-hospital mortality. In-hospital mortality associated with AKI from ATN and nephrotoxins ranged from a low of 24% to a high of 62%. Substantial differences in process of care were also evident across the five sites (e.g. medication use, dialytic modality, timing of initiation of dialysis). Despite the many differences, however, the presumed causes of AKI were relatively similar among institutions. Fully half of patients were labeled as having ATN with no specified precipitant. The next most common causes included nephrotoxin administration (26%), cardiac disease (20%, including myocardial infarction, cardiogenic shock, and congestive heart failure), ATN from hypotension (20%), ATN from sepsis (19%), unresolved prerenal factors (16%) and liver disease (11%).

The largest and most inclusive cohort study of AKI to date was conducted by the Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) investigators [6••]. They prospectively studied patients admitted to 54 intensive care units across 23 countries over 15 months, beginning in September 2000. The study population was patients with severe AKI: inclusion criteria were treatment with renal replacement therapy or AKI defined as oliguria of less than 200 ml in 12 h or blood urea nitrogen (BUN) of more than 84 mg/dl. Of 29 269 patients admitted to the intensive care units, 5.7% had AKI. Similar to the PICARD experience, 30% had preexisting chronic kidney disease (CKD) not requiring dialysis. The most common causes of AKI were septic shock (48%), major surgery (34%), cardiogenic shock (27%), hypovolemia (26%) and nephrotoxin administration (19%). (Multiple causes were allowed on the data collection form, accounting for the sum >100%.)

The overall in-hospital mortality rate in the BEST Kidney cohort study was 60%. As with PICARD, mortality varied widely across centers. Among countries contributing more than 100 patients to the cohort, in-hospital mortality ranged from 51 to 77%. A multivariable logistic regression model to identify independent correlates of in-hospital mortality yielded several previously identified risk factors also found in PICARD [7] or the French Study Group [4], including delayed AKI, age, sepsis and a generic disease severity score that included both BUN and urine output.

Administrative database studies

Medical administrative and claims databases afford investigators the opportunity to study AKI in vast numbers of patients over multiple years admitted to a wide spectrum of hospitals, including those not ordinarily represented in prospective cohort studies. The major limitation of most administrative databases is the lack of detailed clinical and laboratory information. Waikar et al. [8] performed a validation study of the accuracy of International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes for acute renal failure using linked administrative and laboratory data from nearly 100 000 patient discharges from three Boston-area teaching hospitals. Compared with a 100% change in serum creatinine during hospitalization, they found the ICD-9-CM code for ARF (584.x) to have high specificity (97.7%) and negative predictive value (96.1%), but low sensitivity (35.4%) and moderate positive predictive value (47.9%). The ICD-9-CM codes for ARF requiring dialysis (584.x +39.95) were very accurate (>90% for each measure) compared with detailed review of 150 charts.

Two studies to date have utilized large administrative or claims databases to study trends in the epidemiology of AKI in the United States. Xue et al. [9••] used inpatient claims data from a 5% sample of Medicare beneficiaries to investigate the incidence and mortality of acute renal failure between 1992 and 2001. Waikar et al. [10••] used the Nationwide Inpatient Sample (NIS) (a nationally representative database of hospital discharges) to study AKI from 1988 to 2002. Using the same ICD-9-CM codes to identify AKI and a similar and partially overlapping study population, the two studies found a marked rise in the incidence and fall in the mortality associated with AKI and AKI requiring dialysis. Among Medicare beneficiaries, the incidence of AKI rose from 14 to 35 per 1000 discharges between 1992 and 2001; in the NIS, which, unlike the Medicare database, includes patients under the age of 65, the incidence of AKI rose from 4 to 21 per 1000 discharges between 1988 and 2002. Both studies showed a statistically significant decline in mortality, in contrast to the prevailing wisdom and a recent systematic review [11], which suggest that mortality rates have remained unchanged over decades. In the NIS study, in-hospital mortality in patients with AKI requiring dialysis (AKI-D) declined from 41% in 1988 to 28% in 2002. Consistently lower mortality over time was seen in every ARF subgroup examined, including sepsis, acute myocardial infarction, pneumonia, coronary artery bypass grafting and cardiac catheterization. The extent to which changes in coding practice for ARF contributed to these trends was not clear.

Liangos et al. [12] used the National Hospital Discharge Survey (NHDS) (a nationally representative hospital discharge database different from the NIS database used by Waikar et al. [10••]) to study AKI in patients admitted in 2001. Using the same diagnosis codes, they reported that 19 per 1000 discharges had AKI, and that 21% died in hospital – virtually identical to the findings in the NIS. Both NIS and NHDS studies documented that patients with AKI have a median length of stay of 7 days, and that approximately a quarter are discharged to skilled nursing facilities. The NHDS study also showed that the development of AKI added 2 days on average to the length of hospital stay, even after adjusting for numerous covariates. Costs attributable to AKI were not reported in the NIS, NHDS or the Medicare analyses. Costs were addressed in a study by Fischer et al. [13] involving administrative data from 23 Massachusetts hospitals. They reported that uncomplicated ARF (i.e. excluding patients in the intensive care unit) had the third highest median direct hospital costs ($2600) after acute myocardial infarction and stroke.

The study from the NIS estimated the incidence of AKI at 288 per 100 000 US population in 2002; the incidence of AKI-D was estimated to be 27 per 100 000 population. Other investigators have performed population-based epidemiology studies and estimated AKI-D rates of 45 per 100 000 (Manchester, UK) [14], 20 per 100 000 (Scotland) [15] and 8 per 100 000 (Australia) [16].

Epidemiology in disease-specific states

Estimates of the incidence of AKI and associated mortality have been performed in numerous conditions, including sepsis, contrast nephropathy, major surgery and nephrotoxic antibiotic administration. Several of the largest studies are summarized in Table 1 [1727,28••,2944]. A striking and consistent finding is the marked increase in mortality associated with the development of AKI. Studies that have identified risk factors for the development of AKI or AKI-D using multivariable regression models are described in Table 2 [7,17,18,2124,28••,31,38,4451]. Attempts at deriving risk factors or prediction rules for AKI-associated mortality are described in Table 3 [6••,7, 19,5157].

Table 1
Incidence and mortality of AKI in selected conditions
Table 2
Predictors of the development of acute kidney injury
Table 3
Predictors of mortality after acute kidney injury

Small changes in serum creatinine

One of the first studies to examine the independent association between AKI and mortality showed that in patients undergoing radiocontrast procedures, an increase in SCr of at least 25% to at least 2 mg/dl was associated with a 5.5-fold higher odds of death, after adjustment for comorbid medical conditions [58]. Recent studies have explored whether the association between AKI and mortality extends to less severe kidney injury, as assessed by smaller increases in SCr. In a consecutive sample of 19 982 adults admitted to an urban medical center, Chertow et al. [59] found that patients with an increase in SCr of just 0.3–0.4 mg/dl had a 70% higher multivariable-adjusted odds of death than patients with little or no change in SCr. Other investigators have reported comparable findings in patients with congestive heart failure [60,61] and those undergoing cardiac surgery [29,30,43,62]. Brown and colleagues [29] studied 1391 undergoing coronary artery bypass grafting (CABG) to investigate the prognostic significance of varying cut-offs for perioperative SCr increases. Compared with patients with less than a 25% change in SCr, those with a 50–99% increase in SCr had a 6.6-fold increased risk of death at 90 days, adjusted for age and sex. They did not find a significant mortality difference in the group with a 25–49% increase in SCr [hazard ratio (HR) 1.80; 95% confidence interval (CI) 0.73–4.44].

In recognition of the potential clinical importance of small changes in kidney function, and the need to standardize definitions of AKI for clinical and research purposes, the Acute Kidney Dialysis Quality Initiative [63] has proposed the RIFLE criteria for the classification of AKI. The RIFLE criteria provide a graded definition of AKI severity, starting at the lowest stage (‘Risk’, defined as oliguria for over 6 h or an increase in SCr of at least 50%). Progressively more severe injury, as defined by an increase in SCr or duration and severity of oliguria, is denoted by ‘Injury’ and ‘Failure’. The final two stages correspond to prolonged need for renal replacement therapy for more than 4 weeks (‘Loss’) or more than 3 months (‘ESRD’).

Whether the RIFLE criteria will be widely adopted in medicine will depend upon the demonstration of its utility and validity. Research has begun on the incidence and prognosis associated with the various stages of RIFLE [6470]. One large study of 5383 intensive care unit admissions at a single center used an integrated database with physiologic and laboratory information to show that over two-thirds of all patients had some evidence of AKI during admission, and that over half of the patients with ‘Risk’ progressed; the hazard ratio for in-hospital mortality according to maximum RIFLE classification was not significant for ‘Risk’, of borderline statistical significance for ‘Injury’ (HR 1.4; 95% CI 1.0–1.9) and significant for ‘Failure’ (HR 2.7; 95% CI 2.0–3.6) [70].

Acute kidney injury in the setting of chronic kidney disease

The fact that an already damaged organ is at heightened risk of acute injury is intuitive. Indeed, elevated baseline SCr has been consistently observed to be a risk factor for the development of AKI in a number of settings, including radiocontrast administration, open heart surgery and sepsis. Patients with CKD constitute a large fraction of patients with AKI in cohort studies. One-third of patients in the PICARD cohort [7] had CKD stage IV or above. Similarly, in the BEST cohort [6••], 30% of patients had CKD (defined as ‘any abnormal serum level of creatinine or creatinine clearance prior to hospitalization’), while 15% had unknown baseline renal function. In the cohort study by Nash et al. [2], 151 of 332 patients with AKI had SCr values above 1.2 at baseline. Interestingly, patients with CKD have been reported to have lower in-hospital mortality than patients without CKD who develop AKI. This finding has been noted in large databases as well as in studies to identify predictors of mortality following AKI. In the NIS study [10••], 22% of patients with CKD and AKI-D died in hospital, compared with 30% of patients without CKD. In the PICARD cohort [7], the presence of stage IV CKD conferred a 43% (95% CI 16–61%) lower adjusted odds of in-hospital mortality; underlying CKD was not associated with lower odds of death after AKI in the BEST-Kidney cohort [6••]. Used as a continuous variable, higher baseline SCr has also been associated with lower mortality in studies examining outcomes following AKI [7,53]. Reasons that may underlie this seemingly paradoxical finding include confounding by malnutrition (and lower SCr values from low muscle mass), and unrecorded differences in disease severity among persons with and without CKD who develop AKI. In other words, a lesser injury (or fewer associated complications) may result in AKI in the setting of underlying CKD. Conversely, underlying CKD appears to increase the risk of nonrecovery after AKI. In a population-based surveillance study of AKI from Calgary [71], among all patients with AKI who required dialysis 1 year following admission, 63% had preexisting CKD (median preadmission SCr 2.6 mg/dl). Similar findings were observed in PICARD (data not shown).


AKI is an increasingly common and potentially catastrophic complication in hospitalized patients. Early observational studies from the 1980s and 1990s established the general epidemiologic features of AKI, including the incidence, prognostic significance and predisposing medical and surgical conditions. Recent multicenter observational cohorts and administrative databases have enhanced our understanding of the overall disease burden of AKI and trends in its epidemiology. An increasing number of clinical studies focusing on specific types of AKI (e.g. in the setting of intravenous contrast, sepsis and major surgery) have provided further details into this heterogeneous syndrome.

Despite an increasingly sophisticated understanding of the epidemiology and pathobiology of AKI, current prevention strategies are inadequate and treatment options outside of renal replacement therapy are nonexistent. New strategies for the prevention and treatment of AKI are desperately needed and should be facilitated by ongoing clinical and basic studies of AKI pathogenesis, biomarker discovery/validation and novel therapeutic approaches.


acute kidney injury
acute kidney injury requiring dialysis
acute renal failure
blood urea nitrogen
coronary artery bypass grafting
confidence interval
chronic kidney disease
hazard ratio
International Classification of Diseases, 9th Revision, Clinical Modification
National Hospital Discharge Survey
Nationwide Inpatient Sample
serum creatinine

References and recommended reading

Papers of particular interest, published within the annual period of review, have been highlighted as:

• of special interest

•• of outstanding interest

Additional references related to this topic can also be found in the Current World Literature section in this issue (p. 293).

1. Hou SH, Bushinsky DA, Wish JB, et al. Hospital-acquired renal insufficiency: a prospective study. Am J Med. 1983;74:243–248. [PubMed]
2. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis. 2002;39:930–936. [PubMed]
3. Liano F, Pascual J. Madrid Acute Renal Failure Study Group. Epidemiology of acute renal failure: a prospective, multicenter, community-based study. Kidney Int. 1996;50:811–818. [PubMed]
4. Brivet FG, Kleinkneckt DJ, Loirat P, Landais PJ. French Study Group on Acute Renal Failure. Acute renal failure in intensive care units: causes, outcome, and prognostic factors of hospital mortality: a prospective, multicenter study. Crit Care Med. 1996;24:192–198. [PubMed]
5. Mehta RL, Pascual MT, Soroko S, et al. Spectrum of acute renal failure in the intensive care unit: the PICARD experience. Kidney Int. 2004;66:1613–1621. [PubMed]
6••. Uchino S, Kellum JA, Bellomo R, et al. Acute renal failure in critically ill patients: a multinational, multicenter study. Jama. 2005;294:813–818. This is the largest prospective cohort of AKI to date, involving 1738 patients with AKI from 54 hospitals in 23 countries. [PubMed]
7. Chertow GM, Soroko SH, Paganini EP, et al. Mortality after acute renal failure: models for prognostic stratification and risk adjustment. Kidney Int. 2006;70:1120–1126. [PubMed]
8. Waikar SS, Wald R, Chertow GM, et al. Validity of international classification of diseases, ninth revision, clinical modification codes for acute renal failure. J Am Soc Nephrol. 2006;17:1688–1694. [PubMed]
9••. Xue JL, Daniels F, Star RA, et al. Incidence and mortality of acute renal failure in Medicare beneficiaries, 1992 to 2001. J Am Soc Nephrol. 2006;17:1135–1142. This study examined ARF in more than 5 million discharges of Medicare beneficiaries between 1992 and 2001. [PubMed]
10••. Waikar SS, Curhan GC, Wald R, et al. Declining mortality in patients with acute renal failure, 1988 to 2002. J Am Soc Nephrol. 2006;17:1143–1150. This study examined trends in ARF epidemiology between 1988 and 2002 using a large nationally representative hospital discharge database of approximately 100 million patients. [PubMed]
11. Ympa YP, Sakr Y, Reinhart K, Vincent JL. Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med. 2005;118:827–832. [PubMed]
12. Liangos O, Wald R, O’Bell JW, et al. Epidemiology and outcomes of acute renal failure in hospitalized patients: a national survey. Clin J Am Soc Nephrol. 2006;1:43–51. [PubMed]
13. Fischer MJ, Brimhall BB, Lezotte DC, et al. Uncomplicated acute renal failure and hospital resource utilization: a retrospective multicenter analysis. Am J Kidney Dis. 2005;46:1049–1057. [PubMed]
14. Hegarty J, Middleton RJ, Krebs M, et al. Severe acute renal failure in adults: place of care, incidence and outcomes. Qjm. 2005;98:661–666. [PubMed]
15. Metcalfe W, Simpson M, Khan IH, et al. Acute renal failure requiring renal replacement therapy: incidence and outcome. Qjm. 2002;95:579–583. [PubMed]
16. Silvester W, Bellomo R, Cole L. Epidemiology, management, and outcome of severe acute renal failure of critical illness in Australia. Crit Care Med. 2001;29:1910–1915. [PubMed]
17. Yegenaga I, Hoste E, Van Biesen W, et al. Clinical characteristics of patients developing ARF due to sepsis/systemic inflammatory response syndrome: results of a prospective study. Am J Kidney Dis. 2004;43:817–824. [PubMed]
18. Hoste EA, Lameire NH, Vanholder RC, et al. Acute renal failure in patients with sepsis in a surgical ICU: predictive factors, incidence, comorbidity, and outcome. J Am Soc Nephrol. 2003;14:1022–1030. [PubMed]
19. Neveu H, Kleinknecht D, Brivet F, et al. Prognostic factors in acute renal failure due to sepsis: results of a prospective multicentre study. The French Study Group on Acute Renal Failure. Nephrol Dial Transplant. 1996;11:293–299. [PubMed]
20. Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective study. Jama. 1995;273:117–123. [PubMed]
21. Marenzi G, Lauri G, Assanelli E, et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol. 2004;44:1780–1785. [PubMed]
22. Mehran R, Aymong ED, Kikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44:1393–1399. [PubMed]
23. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105:2259–2264. [PubMed]
24. McCullough PA, Wolyn R, Rocher LL, et al. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med. 1997;103:368–375. [PubMed]
25. Mitchell AM, Kline JA. Contrast nephropathy following computed tomography angiography of the chest for pulmonary embolism in the emergency department. J Thromb Haemost. 2007;5:50–54. [PubMed]
26. Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both: a prospective controlled study. N Engl J Med. 1989;320:143–149. [PubMed]
27. Cramer BC, Parfrey PS, Hutchinson TA, et al. Renal function following infusion of radiologic contrast material: a prospective controlled study. Arch Intern Med. 1985;145:87–89. [PubMed]
28••. Mehta RH, Grab JD, O’Brien SM, et al. Bedside tool for predicting the risk of postoperative dialysis in patients undergoing cardiac surgery. Circulation. 2006;114:2208–2216. quiz 2208. The largest study to date to examine predictors of ARF requiring dialysis in patients undergoing coronary artery bypass grafting. The data source was the Society of Thoracic Surgeons National Database. [PubMed]
29. Brown JR, Cochran RP, Dacey LJ, et al. Perioperative increases in serum creatinine are predictive of increased 90-day mortality after coronary artery bypass graft surgery. Circulation. 2006;114 (1 Suppl):I409–I413. [PubMed]
30. Loef BG, Epema AH, Smilde TD, et al. Immediate postoperative renal function deterioration in cardiac surgical patients predicts in-hospital mortality and long-term survival. J Am Soc Nephrol. 2005;16:195–200. [PubMed]
31. Thakar CV, Worley S, Arrigain S, et al. Influence of renal dysfunction on mortality after cardiac surgery: modifying effect of preoperative renal function. Kidney Int. 2005;67:1112–1119. [PubMed]
32. Bove T, Calabro MG, Landoni G, et al. The incidence and risk of acute renal failure after cardiac surgery. J Cardiothorac Vasc Anesth. 2004;18:442–445. [PubMed]
33. Ryckwaert F, Boccara G, Frappier JM, Colson PH. Incidence, risk factors, and prognosis of a moderate increase in plasma creatinine early after cardiac surgery. Crit Care Med. 2002;30:1495–1498. [PubMed]
34. Chertow GM, Lazarus JM, Christiansen CL, et al. Preoperative renal risk stratification. Circulation. 1997;95:878–884. [PubMed]
35. Mangano CM, Diamondstone LS, Ramsay JG, et al. Renal dysfunction after myocardial revascularization: risk factors, adverse outcomes, and hospital resource utilization. The Multicenter Study of Perioperative Ischemia Research Group. Ann Intern Med. 1998;128:194–203. [PubMed]
36. Fowler VG, Jr, Boucher HW, Corey GR, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. 2006;355:653–665. [PubMed]
37. Bates DW, Su L, Yu DT, et al. Mortality and costs of acute renal failure associated with amphotericin B therapy. Clin Infect Dis. 2001;32:686–693. [PubMed]
38. Bates DW, Su L, Donghui T, et al. Correlates of acute renal failure in patients receiving parenteral amphotericin B. Kidney Int. 2001;60:1452–1459. [PubMed]
39. Wingard JR, Kubilis P, Lee L, et al. Clinical significance of nephrotoxicity in patients treated with amphotericin B for suspected or proven aspergillosis. Clin Infect Dis. 1999;29:1402–1407. [PubMed]
40. Leehey DJ, Braun BI, Tholl DA, et al. Can pharmacokinetic dosing decrease nephrotoxicity associated with aminoglycoside therapy. J Am Soc Nephrol. 1993;4:81–90. [PubMed]
41. Smith CR, Lipsky JJ, Laskin OL, et al. Double-blind comparison of the nephrotoxicity and auditory toxicity of gentamicin and tobramycin. N Engl J Med. 1980;302:1106–1109. [PubMed]
42. Prinssen M, Verhoeven EL, Buth J, et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2004;351:1607–1618. [PubMed]
43. Ryckwaert F, Alric P, Picot MC, et al. Incidence and circumstances of serum creatinine increase after abdominal aortic surgery. Intensive Care Med. 2003;29:1821–1824. [PubMed]
44. Godet G, Fleron MH, Vicaut E, et al. Risk factors for acute postoperative renal failure in thoracic or thoracoabdominal aortic surgery: a prospective study. Anesth Analg. 1997;85:1227–1232. [PubMed]
45. Davidson CJ, Hlatky M, Morris KG, et al. Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterisation: a prospective trial. Ann Intern Med. 1989;110:119–124. [PubMed]
46. Rich MW, Crecelius CA. Incidence, risk factors, and clinical course of acute renal insufficiency after cardiac catheterization in patients 70 years of age or older: a prospective study. Arch Intern Med. 1990;150:1237–1242. [PubMed]
47. Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors. AJR Am J Roentgenol. 1991;157:49–58. [PubMed]
48. Gruberg L, Mehran R, Dangas G, et al. Acute renal failure requiring dialysis after percutaneous coronary interventions. Catheter Cardiovasc Interv. 2001;52:409–416. [PubMed]
49. Chertow GM, Levy EM, Hammermeister KE, et al. Independent association between acute renal failure and mortality following cardiac surgery. Am J Med. 1998;104:343–348. [PubMed]
50. Chawla LS, Abell L, Mazhari R, et al. Identifying critically ill patients at high risk for developing acute renal failure: a pilot study. Kidney Int. 2005;68:2274–2280. [PubMed]
51. Chertow GM, Lazarus JM, Paganini EP, et al. Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. The Auriculin Anaritide Acute Renal Failure Study Group. J Am Soc Nephrol. 1998;9:692–698. [PubMed]
52. Liano F, Gallego A, Pascual J, et al. Prognosis of acute tubular necrosis: an extended prospectively contrasted study. Nephron. 1993;63:21–31. [PubMed]
53. Chertow GM, Christiansen CL, Cleary PD, et al. Prognostic stratification in critically ill patients with acute renal failure requiring dialysis. Arch Intern Med. 1995;155:1505–1511. [PubMed]
54. Paganini EP, Halstenberg WK, Goormastic M. Risk modeling in acute renal failure requiring dialysis: the introduction of a new model. Clin Nephrol. 1996;46:206–211. [PubMed]
55. Metnitz PG, Krenn CG, Steltzer H, et al. Effect of acute renal failure requiring renal replacement therapy on outcome in critically ill patients. Crit Care Med. 2002;30:2051–2058. [PubMed]
56. Mehta RL, Pascual MT, Gruta CG, et al. Refining predictive models in critically ill patients with acute renal failure. J Am Soc Nephrol. 2002;13:1350–1357. [PubMed]
57. Lins RL, Elseviers MM, Daelemans R, et al. Re-evaluation and modification of the Stuivenberg Hospital Acute Renal Failure (SHARF) scoring system for the prognosis of acute renal failure: an independent multicentre, prospective study. Nephrol Dial Transplant. 2004;19:2282–2288. [PubMed]
58. Levy EM, Viscoli CM, Horwitz RI. The effect of acute renal failure on mortality: a cohort analysis. Jama. 1996;275:1489–1494. [PubMed]
59. Chertow GM, Burdick E, Honour M, et al. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16:3365–3370. [PubMed]
60. Gottlieb SS, Abraham W, Butler J, et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail. 2002;8:136–141. [PubMed]
61. Smith GL, Vaccarino V, Kosiborod M, et al. Worsening renal function: what is a clinically meaningful change in creatinine during hospitalization with heart failure? J Card Fail. 2003;9:13–25. [PubMed]
62. Lassnigg A, Schmidlin D, Mouhieddine M, et al. Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort study. J Am Soc Nephrol. 2004;15:1597–1605. [PubMed]
63. Kellum JA, Bellomo R, Ronco C, et al. The 3rd International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Int J Artif Organs. 2005;28:441–444. [PubMed]
64. Abosaif NY, Tolba YA, Heap M, et al. The outcome of acute renal failure in the intensive care unit according to RIFLE: model application, sensitivity, and predictability. Am J Kidney Dis. 2005;46:1038–1048. [PubMed]
65. Bell M, Liljestam E, Granath F, et al. Optimal follow-up time after continuous renal replacement therapy in actual renal failure patients stratified with the RIFLE criteria. Nephrol Dial Transplant. 2005;20:354–360. [PubMed]
66. Guitard J, Cointault O, Kamar N, et al. Acute renal failure following liver transplantation with induction therapy. Clin Nephrol. 2006;65:103–112. [PubMed]
67. Heringlake M, Knappe M, Vargas Hein O, et al. Renal dysfunction according to the ADQI–RIFLE system and clinical practice patterns after cardiac surgery in Germany. Minerva Anestesiol. 2006;72:645–654. [PubMed]
68. Kuitunen A, Vento A, Suojaranta-Ylinen R, Pettila V. Acute renal failure after cardiac surgery: evaluation of the RIFLE classification. Ann Thorac Surg. 2006;81:542–546. [PubMed]
69. O’Riordan A, Wong V, McQuillan R, et al. Acute renal disease, as defined by the RIFLE criteria, post-liver transplantation. Am J Transplant. 2006;7:168–176. [PubMed]
70. Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. Crit Care. 2006;10:R73. [PMC free article] [PubMed]
71. Bagshaw SM, Laupland KB, Doig CJ, et al. Prognosis for long-term survival and renal recovery in critically ill patients with severe acute renal failure: a population-based study. Crit Care. 2005;9:R700–R709. [PMC free article] [PubMed]
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