Malakar S, Rungta S, Samanta A, Shamsul Hoda U, Mishra P, Pande G, Roy A, Giri S, Rai P, Mohindra S, Ghoshal UC. Understanding acute kidney injury in cirrhosis: Current perspective. World J Hepatol 2025; 17(5): 104724 [DOI: 10.4254/wjh.v17.i5.104724]
Corresponding Author of This Article
Sumit Rungta, Department of Medical Gastroenterology, King George's Medical University, Chowk, Lucknow 226003, Uttar Pradesh, India. drsumitrungta79@gmail.com
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/
Sayan Malakar, Department of Gastroenterology, King George's Medical University, Lucknow 226003, Uttar Pradesh, India
Sumit Rungta, Department of Medical Gastroenterology, King George's Medical University, Lucknow 226003, Uttar Pradesh, India
Arghya Samanta, Department of Pediatric Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, Uttar Pradesh, India
Umair Shamsul Hoda, Piyush Mishra, Gaurav Pande, Praveer Rai, Samir Mohindra, Uday C Ghoshal, Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, Uttar Pradesh, India
Akash Roy, Department of Gastrosciences and Liver Transplantation, Apollo Multispeciality Hospitals, Kolkata 700054, West Bengal, India
Suprabhat Giri, Department of Gastroenterology and Hepatology, Kalinga Institute of Medical Sciences, Bhubaneswar 751024, Odisha, India
Author contributions: Malakar S, Mishra P, Hoda US, Pande G, and Rungta S contributed to the preparation of the manuscript; Roy A, Samanta A, Ghoshal UC, Mohindra S, Rai P, and Giri S contributed to the supervision of the project, revision of the manuscript, and intellectual input; Malakar S, Hoda US, and Mishra P contributed to preparation of the final draft.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
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: Sumit Rungta, Department of Medical Gastroenterology, King George's Medical University, Chowk, Lucknow 226003, Uttar Pradesh, India. drsumitrungta79@gmail.com
Received: December 31, 2024 Revised: March 13, 2025 Accepted: April 15, 2025 Published online: May 27, 2025 Processing time: 148 Days and 15 Hours
Abstract
Acute kidney injury (AKI) is present in 30%-40% of hospitalized patients with cirrhosis. Its incidence is higher in patients with severe alcoholic hepatitis, spontaneous bacterial peritonitis, and acute-on-chronic-liver failure (ACLF). Kidney injury is an important landmark event in the natural history of cirrhosis as it is associated with higher mortality. Overwhelming systemic vasodilation, cardiac dysfunction, hypoperfusion, endotoxemia, and direct nephrotoxicity predispose patients with cirrhosis to kidney injury. Infection is present in 25% of patients with decompensated cirrhosis and 35%-40% of patients with ACLF. Advanced cirrhosis with portal hypertension leads to a sluggish portal flow, leading to increased gut congestion, altered gut permeability and bacterial translocations. They drive infection and endotoxemia in such patients. Pathogen-associated molecular patterns activate inflammatory cascades, which leads to further deterioration in hemodynamics and reduced glomerular filtration rate. Infections and pro-inflammatory cytokines like interleukin 6 (IL-6), IL-1, and tumor necrosis factor alpha may directly cause kidney parenchymal injury. The combined effect of dysfunctional albumin and systemic and splanchnic vasodilatation leads to low effective blood volume, activating the renin-angiotensin-aldosterone system. This causes renal vasoconstriction, water retention, and ascites, which progresses to hepatorenal physiology and AKI development. Vasoconstriction and volume expansion effectively improve arterial blood volume and systemic hemodynamics, thereby improving renal blood flow. It is of paramount importance to predict, detect, and treat AKI in its early state, as progressive renal dysfunction is invariably associated with higher mortality in patients with decompensated cirrhosis and ACLF. This comprehensive review will focus on the recent evolving concepts of the pathophysiology, diagnosis, and management of AKI in patients with cirrhosis.
Core Tip: The development of acute kidney injury (AKI) changes the trajectory of the natural history of patients with decompensated cirrhosis or acute-on-chronic-liver failure. With the discovery of newer biomarkers and a better understanding of hemodynamics in patients with AKI and cirrhosis, there is a paradigm shift in the management of such patients. This comprehensive review focuses on the current perspective of the pathophysiology, diagnosis, and management of patients with AKI in cirrhosis.
