Le syndrome hépatorénal en 2025

Abstract

Acute kidney injury (AKI) affects 20 to 50% of hospitalized cirrhotic patients, reaching up to 58% in intensive care settings. The recent alignment of diagnostic criteria with KDIGO standards has enabled earlier and standardized identification. Hepatorenal syndrome (HRS), accounting for 12% of AKI cases, arises from complex mechanisms combining splanchnic vasodilation related to portal hypertension, effective hypovolemia, activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, intrarenal vasoconstriction, and a reduction in glomerular filtration rate. These processes are further exacerbated by inflammatory phenomena and bacterial translocation. HRS-AKI is defined as a functional impairment that does not improve after discontinuation of diuretics and 24 hours of volume expansion, in the absence of other identifiable AKI causes. However, its diagnosis remains challenging in intensive care due to the numerous renal insults encountered in this population. The treatment is based on the administration of terlipressin and albumin, with liver transplantation being the only curative option. Although vasoconstrictors temporarily improve renal function, their use should be regarded as a bridge to liver transplantation or renal recovery. In the future, the integration of biomarkers, refined diagnostic criteria, and innovative therapeutic strategies will be crucial to optimize the management and prognosis of these high-risk patients.