Kidney injury in cirrhosis: pathophysiological and therapeutic aspects of hepatorenal syndromes


  • Søren Møller,

    Corresponding author
    1. Department of Clinical Physiology 239, Center of Functional and Diagnostic Imaging and Research, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark
    • Correspondence

      Søren Møller, MD, Dr.MSc., Professor, Department of Clinical Physiology, 239 Hvidovre Hospital DK-2650, Hvidovre, Denmark

      Tel: +45 3862 3568

      Fax: +45 3862 3750


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  • Aleksander Krag,

    1. Department of Medical Gastroenterology, Odense University Hospital, Odense, Denmark
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  • Flemming Bendtsen

    1. Gastro Unit Medical Division 360, Faculty of Health Sciences, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark
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Acute kidney injury (AKI) is frequent in patients with cirrhosis. AKI and hyponatraemia are major determinants of the poor prognosis in advanced cirrhosis. The hepatorenal syndrome (HRS) denotes a functional and potential reversible impairment of renal function. Type 1 HRS, a special type of AKI, is a rapidly progressive AKI, whereas the renal function in type 2 HRS decreases more slowly. HRS is precipitated by factors such as sepsis that aggravate the effective hypovolaemia in decompensated cirrhosis, by lowering arterial pressure and cardiac output and enhanced sympathetic nervous activity. Therefore, attempts to prevent and treat HRS should seek to improve liver function and to ameliorate arterial hypotension, central hypovolaemia and cardiac output, and to reduce renal vasoconstriction. Ample treatment of HRS is important to prevent further progression and death, but as medical treatment only modestly improves long-term survival, these patients should always be considered for liver transplantation. Hyponatraemia, defined as serum sodium <130 mmol/L, is common in patients with decompensated cirrhosis. From a pathophysiological point of view, hyponatraemia is related to an impairment of renal solute-free water excretion most likely caused by an increased vasopressin secretion. Patients with cirrhosis mainly develop hypervolaemic hyponatraemia. Current evidence does not support routine use of vaptans in the management of hyponatraemia in cirrhosis.