Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

Acute kidney injury in cirrhosis

implications for liver transplantation

MacDonald, Andrew J.a; Nadim, Mitra K.b; Durand, Françoisc,d; Karvellas, Constantine J.e,f

Current Opinion in Critical Care: April 2019 - Volume 25 - Issue 2 - p 171–178
doi: 10.1097/MCC.0000000000000590
GASTROINTESTINAL SYSTEM: Edited by Constantine J. Karvellas
Buy
SDC

Purpose of review Acute kidney injury (AKI) in cirrhosis consists of varying phenotypes, with hepatorenal syndrome (HRS) representing a single entity. Prompt recognition and diagnosis of AKI cause identifies appropriate therapeutic measures. This review provides an overview of AKI definitions, highlights challenges in quantifying renal impairment in cirrhosis, lists novel diagnostic AKI biomarkers, and summarizes transplantation implications.

Recent findings Biomarkers (neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, interleukin-18, and liver-type fatty acid-binding protein) may assist in the identification of underlying acute tubular necrosis. Of these, neutrophil gelatinase-associated lipocalin is the most promising; however, significant overlap occurs among AKI phenotypes, with diagnostic values yet to be defined. Mainstay treatment of HRS consists of albumin and vasopressors. Acute-on-chronic liver failure grade independently predicts response to terlipressin treatment. Many end-stage liver disease patients with AKI have underlying chronic kidney disease with important implications on pre and postliver transplantation mortality. Simultaneous liver–kidney transplant candidacy is based on low likelihood of renal recovery.

Summary Novel biomarkers may assist in identification of acute tubular necrosis and persistent/severe AKI. Norepinephrine has been suggested to be inferior to terlipressin, with additional research required. Increasing acute-on-chronic liver failure grade correlates with lower likelihood of vasopressor response in HRS. Severe preliver transplantation AKI confers significantly worse postliver transplantation renal outcomes.

aDivision of General Surgery, University of Alberta, Edmonton, Alberta, Canada

bDivision of Nephrology & Hypertension, Department of Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA

cHepatology & Liver Intensive Care Unit, Hospital Beaujon, Clichy

dINSERM U1149 and University Paris VII, Denis Diderot, Paris, France

eDepartment of Critical Care Medicine

fDivision of Gastroenterology (Liver Unit), University of Alberta, Edmonton, Alberta, Canada

Correspondence to Constantine J. Karvellas, MD, SM, FRCPC, FCCM, Division of Gastroenterology (Liver Unit), Department of Critical Care Medicine, University of Alberta, 1-40 Zeidler Ledcor Building, Edmonton, AB T6G 2X8, Canada. Tel: +780 492 4390; e-mail: dean.karvellas@ualberta.ca

Copyright © 2019 YEAR Wolters Kluwer Health, Inc. All rights reserved.