Kidney Week Educational Symposia-Caring for the Patient with AKI in Cirrhosis: New Tools and Opportunities

Video Transcription

Video Summary

The symposium opens with nephrologist Andrew Davenport (UCL) introducing hepatorenal syndrome (HRS) as the poorest-prognosis cause of acute kidney injury (AKI) in cirrhosis. He explains why serum creatinine underestimates renal dysfunction in liver disease: reduced creatine intake/production, sarcopenia and inactivity lowering creatinine generation, dilution from ascites, and lab interference from bilirubin (even with enzymatic assays). These factors delay or blunt creatinine rises, complicating AKI recognition. He also challenges the idea of HRS as purely “functional,” highlighting evidence of tubular inflammation (TLR2/4 upregulation), ischemic changes, and apoptosis—suggesting delayed treatment can progress to acute tubular injury.<br /><br />Lewis Junkers (University of Arkansas) focuses on diagnosing and monitoring HRS-AKI. He reviews ICA/KDIGO-based criteria (with discussion of adding urine output, which predicts outcomes) and emphasizes that “AKI in cirrhosis ≠ HRS.” Differentiation among volume-responsive pre-renal states, non–volume-responsive causes (including HRS), acute tubular injury, cardio-renal contributions, and intra-abdominal hypertension is essential. Traditional indices (FENa, albuminuria) and biomarkers (e.g., NGAL) help mainly at extremes due to overlap. He argues for better hemodynamic/volume assessment (e.g., point-of-care ultrasound, abdominal perfusion pressure) to avoid harm from empiric albumin in already overloaded patients, and presents ICU experience suggesting some refractory cases improve when cardiac dysfunction and congestion are addressed.<br /><br />Hepatologist Guadalupe Garcia-Tsao (Yale) frames HRS-AKI as a hallmark of “further decompensation” in cirrhosis with ascites, driven by portal hypertension, vasodilation, and inflammation (often infection/SBP). She reviews management: stop precipitating factors, assess volume carefully, give albumin selectively, and treat HRS-AKI with vasoconstrictors plus albumin—terlipressin preferred (norepinephrine second-line; midodrine/octreotide low efficacy). She highlights pulmonary edema risk and suggests continuous terlipressin infusion may reduce adverse events. Definitive therapy remains expedited liver transplant. Q&A centers on paracentesis/albumin, volume assessment challenges, BNP limits, terlipressin cost, hyponatremia, and dialysis decisions.

Asset Subtitle

Moderator(s): Andrew Davenport

Presentation(s):

Introduction - Andrew Davenport
Diagnosing and Monitoring HRS-AKI: Present and Future - Luis Juncos
How Hepatologists Think About HRS-AKI Treatment in 2023 - Guadalupe Garcia-Tsao

Support is provided by an educational grant from Mallinckrodt Pharmaceuticals.

Meta Tag

Date 11/3/2023

Pathway 1 AKI and Critical Care

Session ID 464916

Session Type ES - Educational Symposium

Keywords

hepatorenal syndrome (HRS)

HRS-AKI in cirrhosis

acute kidney injury (AKI) diagnosis

serum creatinine limitations in liver disease

sarcopenia and creatinine underestimation

bilirubin assay interference

tubular inflammation and acute tubular injury

ICA/KDIGO criteria and urine output

volume assessment (POCUS) and hemodynamics

terlipressin plus albumin therapy

liver transplantation for HRS