Kidney Week

Abstract: TH-PO0770

Echocardiographic Correlates of Vasoconstrictor Treatment Response in Hepatorenal Syndrome-AKI

Session Information

• AKI: Critical Care, CKRT, Cardiorenal Syndromes, and Clinical Outcomes
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

• 102 AKI: Clinical, Outcomes, and Trials

Authors

• Patel, Neev, Stanford Medicine, Stanford, California, United States

Neev Patel, MD

• Rajasekaran, Vignesh, Stanford Medicine, Stanford, California, United States

Vignesh Rajasekaran, MD

• Izzy, Manhal J., Vanderbilt University Medical Center, Nashville, Tennessee, United States

Manhal J. Izzy, MD

• Teixeira, J. Pedro, The University of New Mexico, Albuquerque, New Mexico, United States

J. Pedro Teixeira, MD, FASN

• Allegretti, Andrew S., Mass General Brigham Inc, Boston, Massachusetts, United States

Andrew S. Allegretti, MD, MS, FASN

• Patidar, Kavish Rohit, Houston Methodist, Houston, Texas, United States

Kavish Rohit Patidar, DO

• Kwong, Allison, Stanford Medicine, Stanford, California, United States

Allison Kwong

• Cheng, Xingxing S., Stanford Medicine, Stanford, California, United States

Xingxing S. Cheng, MD, MS

Background

Vasoconstrictor therapy is the only effective pharmacologic treatment for hepatorenal syndrome-acute kidney injury (HRS-AKI), yet response is variable and predictors remain poorly defined. We assessed whether pre-treatment echocardiographic parameters are associated with vasoconstrictor response.

Methods

Single-center retrospective study of HRS-AKI patients treated with terlipressin or norepinephrine with pre-treatment transthoracic echocardiography within 90 days. Response was defined by International Club of Ascites (ICA) criteria (complete or partial). Each echocardiographic parameter was modeled by linear regression on response, vasoconstrictor type, and their interaction.

Results

Of 94 patients, 63 had pre-treatment echocardiography (26 terlipressin, 31 norepinephrine, 6 crossover); 19 (30%) responded by ICA criteria. Pre-treatment RVSP (37 vs 28 mm Hg; p=0.02) and TR velocity (2.7 vs 2.4 m/sec; p=0.03) were higher in responders. Diastolic indices (lateral/septal e′, E/e′, LAVI) and LVEF (65 vs 66%) did not differ; no vasoconstrictor × response interaction was observed. Cirrhotic cardiomyopathy (Consortium criteria, 50/63 evaluable) was present in 0/12 responders vs 3/38 non-responders (p=1.00).

Conclusion

Higher pre-treatment RVSP and TR velocity, but not diastolic indices or LVEF, were associated with ICA response to vasoconstrictor therapy in HRS-AKI, with no differential effect by drug. Given the limited sample size, these hypothesis-generating findings warrant validation in a multicenter cohort.