Kidney Week 2025 Annual Meeting-AKI and Hepatorenal Syndrome: Diagnosis, Management, and Treatment

Video Transcription

Video Summary

This educational session focused on acute kidney injury (AKI) in cirrhosis and hepatorenal syndrome (HRS), emphasizing how difficult diagnosis is and how management depends on identifying the dominant mechanism. Dr. Ayesha Arikan introduced two speakers: Dr. Andrew Allegretti on HRS pathophysiology and Dr. Kianush Kashani on diagnosis and treatment.<br /><br />Dr. Allegretti described three contributors to kidney dysfunction in cirrhosis: (1) circulatory/hemodynamic dysfunction (the core “peripheral arterial vasodilation” model driven by portal hypertension, reduced effective arterial volume, and neurohormonal activation causing renal vasoconstriction), (2) tubular injury (often overlapping with HRS), and (3) systemic/microcirculatory inflammation. He reviewed the historical evolution of HRS as a “functional” renal failure and highlighted limitations of creatinine in cirrhosis due to sarcopenia; cystatin C may improve assessment but lacks AKI staging criteria. He discussed diagnostic support tools including fractional excretion of sodium and urinary biomarkers, especially NGAL, which can help distinguish HRS from ATN and add prognostic value. He also noted emerging inflammatory targets (e.g., angiopoietin-2) that may predict treatment response.<br /><br />Dr. Kashani reviewed modern definitions: AKI in cirrhosis now uses KDIGO criteria including urine output; HRS categories include HRS-AKI, HRS-acute kidney disease, and HRS-CKD. He emphasized that urine output predicts mortality similarly to creatinine changes. Diagnostic approach includes careful history, volume/hemodynamic assessment (including ultrasound), urine indices/sediment, and biomarkers; kidney biopsy studies show frequent structural lesions despite “HRS-like” clinical presentations, supporting a continuum rather than a binary HRS vs ATN model.<br /><br />Management priorities include stopping nephrotoxins, treating infection (including diagnostic paracentesis), optimizing effective volume, and using albumin plus vasoconstrictors when HRS-AKI is suspected. Terlipressin improves HRS reversal but carries respiratory failure risk; norepinephrine is an alternative. A debated point was diuretics: Kashani argued against routinely stopping them, suggesting loop diuretics with vasopressors can improve urine output without worsening creatinine, while MRAs are often held during rising creatinine. The Q&A covered NGAL thresholds (~200–250 for HRS vs ATN in studies), cautious use of tolvaptan due to hepatotoxicity warnings, limited evidence for SGLT2 inhibitors in low GFR states, and the value of echocardiography/POCUS to assess cardiomyopathy and volume status before/while treating HRS.

Asset Subtitle

Moderator(s): Ayse Akcan Arikan

Presentation(s):

Introduction - Ayse Akcan Arikan
Pathophysiology of HRS-AKI - Andrew Allegretti
Diagnosis and Management of Acute Kidney Dysfunction in Cirrhosis - Kianoush Kashani

Support is provided by an educational grant from Mallinckrodt Pharmaceuticals.

Meta Tag

Date 11/8/2025

Pathway 1 AKI and Critical Care

Session ID 519710

Keywords

acute kidney injury

cirrhosis

hepatorenal syndrome

HRS-AKI

KDIGO criteria

peripheral arterial vasodilation

renal vasoconstriction

NGAL biomarker

acute tubular necrosis

albumin and vasoconstrictors

terlipressin