4.6 Article

Pathogenesis of Hepatorenal Syndrome: Implications for Therapy

Journal

AMERICAN JOURNAL OF KIDNEY DISEASES
Volume 67, Issue 2, Pages 318-328

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.ajkd.2015.09.013

Keywords

Hepatorenal syndrome (HRS); cirrhosis; acute kidney injury (AKI); biomarkers; liver transplantation; pathophysiology; simultaneous liver-kidney transplantation; vasoconstrictor drugs; renal function; review

Funding

  1. Instituto de Salud Carlos III
  2. Fondo de Investigacion (FIS) Instituto de Salud Carlos III [FIS 12/00330]
  3. Fondo Europeo de Desarrollo Regional (FEDER). Union Europea

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Patients with cirrhosis are prone to develop acute kidney injury (AKI) due to a number of causes, including bacterial infections with or without septic shock, hypovolemia, administration of nephrotoxic drugs, and intrinsic kidney diseases, among others. Most importantly, patients with advanced cirrhosis develop a distinctive cause of AKI, characterized by rapidly progressive glomerular filtration rate loss associated with marked disturbances in circulatory function in the absence of obvious pathologic abnormalities in the kidneys, known as hepatorenal syndrome (HRS). Decreased kidney function results from intense renal vasoconstriction secondary to the complex circulatory changes of cirrhosis with splanchnic vasodilatation and effective hypovolemia. Beyond activation of vasoactive systems, factors including impaired renal blood flow autoregulation and systemic inflammation may play a role in the development of HRS. Most patients improve with albumin and vasopressors; however, the prognosis of HRS remains very poor. Novel biomarkers may be helpful in distinguishing HRS from other causes of AKI in patients with cirrhosis. (C) 2016 by the National Kidney Foundation, Inc.

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