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Semin Respir Crit Care Med 2011; 32(5): 639-650
DOI: 10.1055/s-0031-1287872
© Thieme Medical Publishers

Acute Renal Failure

Rinaldo Bellomo1 , 2 , 3 , 4
  • 1Department of Intensive Care, Austin Hospital, Melbourne, Victoria, Australia
  • 2Department of Medicine, Austin Hospital, Melbourne, Victoria, Australia
  • 3Department of Intensive Care, Melbourne University, Melbourne, Victoria, Australia
  • 4Department of Medicine, Melbourne University, Melbourne, Victoria, Australia
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Publikationsdatum:
11. Oktober 2011 (online)

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ABSTRACT

Acute renal failure (now acute kidney injury) is a common complication of critical illness affecting between 30 and 60% of critically ill patients. The development of a consensus definition (RIFLE—risk, injury, failure, loss, end-stage system) has allowed standardization of reporting and epidemiological work. Multicenter multinational epidemiological studies indicate that sepsis is now the most common cause of acute renal failure in the intensive care unit (ICU) followed by cardiac surgery–associated acute kidney injury. Unfortunately, our understanding of the pathogenesis of acute renal failure in these settings remains limited. Because of such limited understanding, no reproducibly effective therapies have been developed. In addition the diagnosis of acute renal failure still rests upon the detection of changes in serum creatinine, which only occur if more than 50% of glomerular filtration is lost and are often delayed by more than 24 hours. Such diagnostic delays make the implementation of early therapy nearly impossible. In response to these difficulties, there has been a concerted effort to use proteomics to identify novel early biomarkers of acute renal failure. The identification and study of neutrophil gelatinase– associated lipocalin has been an important step in this field. Another area of active interest and investigation relates to the role of intravenous fluid resuscitation and fluid balance. Data from large observational studies and randomized, controlled trials consistently indicate that a positive fluid balance in patients with acute renal failure represents a major independent risk factor for mortality and provides no protection of renal function. The pendulum is clearly swinging away from a fluid-liberal approach to a fluid-conservative approach in these patients. Finally, there is a growing appreciation that acute renal failure may identify patients who are at increased risk of subsequent chronic renal dysfunction and mortality, opening the way to post-ICU interventional trials.

KEYWORDS

Acute renal failure - acute kidney injury - acute tubular necrosis - creatinine - renal replacement therapy

REFERENCES

Rinaldo BellomoM.B.B.S. M.D. 

Australian and New Zealand Intensive Care Research Centre, Monash University School of Public Health and Preventive Medicine

Commercial Rd., Prahran, Melbourne, Victoria 3084, Australia

eMail: rinaldo.bellomo@austin.org.au