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Review
. 2021 Jul 14;27(26):3984-4003.
doi: 10.3748/wjg.v27.i26.3984.

Acute kidney injury and hepatorenal syndrome in cirrhosis

Kapil Gupta  1 , Abhishek Bhurwal  1 , Cindy Law  1 , Scott Ventre  2 , Carlos D Minacapelli  1 , Savan Kabaria  2 , You Li  1 , Christopher Tait  1 , Carolyn Catalano  1 , Vinod K Rustgi  3
Affiliations
Review

Acute kidney injury and hepatorenal syndrome in cirrhosis

Kapil Gupta et al. World J Gastroenterol. .

Abstract

Acute kidney injury (AKI) in cirrhosis, including hepatorenal syndrome (HRS), is a common and serious complication in cirrhotic patients, leading to significant morbidity and mortality. AKI is separated into two categories, non-HRS AKI and HRS-AKI. The most recent definition and diagnostic criteria of AKI in cirrhosis and HRS have helped diagnose and prognosticate the disease. The pathophysiology behind non-HRS-AKI and HRS is more complicated than once theorized and involves more processes than just splanchnic vasodilation. The common biomarkers clinicians use to assess kidney injury have significant limitations in cirrhosis patients; novel biomarkers being studied have shown promise but require further studies in clinical settings and animal models. The overall management of non-HRS AKI and HRS-AKI requires a systematic approach. Although pharmacological treatments have shown mortality benefit, the ideal HRS treatment option is liver transplantation with or without simultaneous kidney transplantation. Further research is required to optimize pharmacologic and nonpharmacologic approaches to treatment. This article reviews the current guidelines and recommendations of AKI in cirrhosis.

Keywords: Acute kidney injury; Biomarkers; Hepatorenal syndrome; Liver cirrhosis; Prognosis; Treatment.

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Conflict of interest statement

Conflict-of-interest statement: There are no relevant financial disclosures or conflicts of interest for all authors.

Figures

Figure 1
Figure 1
Pathogenesis of hepatorenal syndrome and acute kidney injury in cirrhosis. (1) Patients with cirrhosis present with a marked splanchnic arterial vasodilation due to portal hypertension; (2) Splanchnic vasodilation causes a decrease in systemic vascular resistance leading to effective arterial hypovolemia; (3) There is activation of endogenous vasoconstrictors such as the renin-angiotensin-aldosterone system, sympathetic nervous system and arginine vasopressin; and (4) The activation of these systems leads to renal vasoconstriction inducing a decrease in glomerular filtration rate and development of hepatorenal syndrome. A decrease in cardiac output may contribute to a decrease in effective arterial blood volume. Pathogen-associated molecular patterns and damage-associated molecular patterns, derived from bacterial translocation and from injured liver, may activate circulating innate immune cells, leading to an inflammatory response. The Inflammatory mediators may lead to impairment of circulatory dysfunction and consequently, kidney tissue damage. Library of Science & Medical Illustrations were utilized in part to create this figure (https://creativecommons.org/Licenses/by-nc-sa/4.0/). DAMPs: Damage-associated molecular patterns; PAMPs: Pathogen-associated molecular patterns.
Figure 2
Figure 2
Algorithm of the diagnosis and treatment of hepatorenal syndrome. The algorithm indicates differential diagnosis, diagnosis of hepatorenal syndrome (HRS) and HRS treatment. Library of Science & Medical Illustrations were utilized in part to create this figure (https://creativecommons.org/Licenses/by-nc-sa/4.0/). Cr: Creatinine; ICA: International club ascites; AKI: Acute kidney injury; HRS: Hepatorenal syndrome; ICU: Intensive care unit; NE: Norepinephrine.
See this image and copyright information in PMC

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