Wu HHL, Athwal VS, Kalra PA, Chinnadurai R. COVID-19 and hepatorenal syndrome. World J Gastroenterol 2022; 28(39): 5666-5678 [PMID: 36338894 DOI: 10.3748/wjg.v28.i39.5666]
Corresponding Author of This Article
Henry H L Wu, MBChB, Academic Editor, Academic Fellow, Doctor, Honorary Research Fellow, Renal Research, Kolling Institute of Medical Research, Royal North Shore Hospital, Reserve Road, 2065 St. Leonards NSW, Sydney 2065, New South Wales, Australia. honlinhenry.wu@health.nsw.gov.au
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Oct 21, 2022; 28(39): 5666-5678 Published online Oct 21, 2022. doi: 10.3748/wjg.v28.i39.5666
COVID-19 and hepatorenal syndrome
Henry H L Wu, Varinder S Athwal, Philip A Kalra, Rajkumar Chinnadurai
Henry H L Wu, Renal Research, Kolling Institute of Medical Research, Royal North Shore Hospital, Sydney 2065, New South Wales, Australia
Varinder S Athwal, Faculty of Biology, Medicine & Health (Division of Diabetes, Metabolism & Gastroenterology), The University of Manchester, Manchester M13 9PL, United Kingdom
Philip A Kalra, Rajkumar Chinnadurai, Department of Renal Medicine, Northern Care Alliance NHS Foundation Trust, Salford M6 8HD, United Kingdom
Author contributions: Wu HHL performed the majority of the writing, prepared the figures and tables; Athwal VS, Kalra PA, and Chinnadurai R provided review of the draft versions of the paper prior to submission of the final version; Wu HHL and Chinnadurai R designed the outline and coordinated the writing of the paper.
Conflict-of-interest statement: The authors report no conflicts of interest associated with the work presented in this manuscript.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Henry H L Wu, MBChB, Academic Editor, Academic Fellow, Doctor, Honorary Research Fellow, Renal Research, Kolling Institute of Medical Research, Royal North Shore Hospital, Reserve Road, 2065 St. Leonards NSW, Sydney 2065, New South Wales, Australia. honlinhenry.wu@health.nsw.gov.au
Received: September 4, 2022 Peer-review started: September 4, 2022 First decision: September 19, 2022 Revised: September 21, 2022 Accepted: September 30, 2022 Article in press: September 30, 2022 Published online: October 21, 2022 Processing time: 43 Days and 22.4 Hours
Abstract
Coronavirus disease 2019 (COVID-19) is a highly infectious disease which emerged into a global pandemic. Although it primarily causes respiratory symptoms for affected patients, COVID-19 was shown to have multi-organ manifestations. Elevated liver enzymes appear to be commonly observed during the course of COVID-19, and there have been numerous reports of liver injury secondary to COVID-19 infection. It has been established that patients with pre-existing chronic liver disease (CLD) are more likely to have poorer outcomes following COVID-19 infection compared to those without CLD. Co-morbidities such as diabetes, hypertension, obesity, cardiovascular and chronic kidney disease frequently co-exist in individuals living with CLD, and a substantial population may also live with some degree of frailty. The mechanisms of how COVID-19 induces liver injury have been postulated. Hepatorenal syndrome (HRS) is the occurrence of kidney dysfunction in patients with severe CLD/fulminant liver failure in the absence of another identifiable cause, and is usually a marker of severe decompensated liver disease. Select reports of HRS following acute COVID-19 infection have been presented, although the risk factors and pathophysiological mechanisms leading to HRS in COVID-19 infection or following COVID-19 treatment remain largely unestablished due to the relative lack and novelty of published data. Evidence discussing the management of HRS in high-dependency care and intensive care contexts is only emerging. In this article, we provide an overview on the speculative pathophysiological mechanisms of COVID-19 induced HRS and propose strategies for clinical diagnosis and management to optimize outcomes in this scenario.
Core Tip: There have been numerous reviews evaluating the causative relationship between coronavirus disease 2019 (COVID-19) and liver pathology, given an emerging number of cases reporting COVID-19 induced liver injury. There are few reports noting the onset of hepatorenal syndrome (HRS) in the face of COVID-19 infection. Occurrence of HRS in any circumstance is typically an indicator of severe and perhaps life-threatening disease, potentially requiring liver transplantation. With a paucity in literature compilation on the associations between COVID-19 and HRS, we provide a review which discusses the purported pathophysiological mechanisms of COVID-19 induced HRS, and propose clinical assessment and management approaches in this scenario.
