Acute kidney injury in cirrhosis

Authors

  • Guadalupe Garcia-Tsao,

    Corresponding author
    1. Section of Digestives Diseases, Yale University School of Medicine, New Haven, CT, and VA-Connecticut Healthcare System, West Haven, CT
    • Yale University School of Medicine, Section of Digestive Diseases, One Gilbert Street, TAC, room # S241B, New Haven, CT 06510
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    • fax: 203-785-7273.

  • Chirag R. Parikh,

    1. Section of Nephrology, Yale University School of Medicine, New Haven, CT and VA-Connecticut Healthcare System, West Haven, CT
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  • Antonella Viola

    1. Section of Digestives Diseases, Yale University School of Medicine, New Haven, CT, and VA-Connecticut Healthcare System, West Haven, CT
    2. Department of Clinical Medicine, University of Bologna, Italy
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  • Potential conflict of interest: Nothing to report.

Abstract

Acute renal failure (ARF), recently renamed acute kidney injury (AKI), is a relatively frequent problem, occurring in approximately 20% of hospitalized patients with cirrhosis. Although serum creatinine may underestimate the degree of renal dysfunction in cirrhosis, measures to diagnose and treat AKI should be made in patients in whom serum creatinine rises abruptly by 0.3 mg/dL or more (≥26.4 μmol/L) or increases by 150% or more (1.5-fold) from baseline. The most common causes of ARF (the term is used interchangeably with AKI) in cirrhosis are prerenal azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a functional type of prerenal AKI exclusive of cirrhosis that does not respond to volume repletion. Because of the progressive vasodilatory state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developing AKI with events associated with a decrease in effective arterial blood volume. HRS can occur spontaneously but is more frequently precipitated by events that worsen vasodilatation, such as spontaneous bacterial peritonitis. Conclusion: Specific therapies of AKI depend on the most likely cause and mechanism. Vasoconstrictors are useful bridging therapies in HRS. Ultimately, liver transplantation is indicated in otherwise reasonable candidates in whom AKI does not resolve with specific therapy. (HEPATOLOGY 2008;48:2064-2077.)

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