Abstract: SA-PO0204
Terlipressin for Sinusoidal Obstruction Syndrome: Expanding Indications Beyond Cirrhotic Hepatorenal Syndrome
Session Information
- Onconephrology: MGRS, HSCT, Electrolytes, RCC, and More
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Meath, Callie J, Baylor College of Medicine, Houston, Texas, United States
- Simon, Bindu, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
- Mehta, Rohtesh S, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
- Kebriaei, Partow, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
- Lin, Jamie S., The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
Introduction
Sinusoidal obstruction syndrome (SOS) is a life-threatening complication of allogeneic hematopoietic cell transplantation (HCT), occurring in 5-15% of cases with mortality rates >80% once multiorgan failure develops. SOS begins with endothelial injury to hepatic sinusoids, leading to portal hypertension and subsequent acute kidney injury. Standard of care treatment often fails, culminating in dialysis dependence. Given hemodynamic parallels with cirrhotic-HRS, terlipressin may benefit SOS-associated renal failure. This is the first reported case of its successful use in this context.
Case Description
A 45-year-old woman with B-cell acute lymphoblastic leukemia underwent matched related donor allogeneic HCT following inotuzumab ozogamicin exposure, placing her at high risk for SOS. She received reduced-intensity conditioning and post-transplant cyclophosphamide. Her post-transplant course was complicated by Streptococcus bacteremia, diarrhea, and SOS. Despite early intervention with defibrotide, diuretics, and supportive care, by day 16 she had gained 17% over dry weight, developed hypotension, anasarca, new oxygen requirements, increasing bilirubin level 2.6 mg/dL (0.0-1.2 mg/dL) and worsening kidney function (creatinine 3.75 mg/dL from baseline 0.89 mg/dL). Imaging revealed hepatic congestion with ascites. Prior to dialysis initiation, she received terlipressin (0.85 mg IV q6h) and continuous bumetanide infusion. Within 24 hours, blood pressure normalized, urine output improved, and creatinine peaked at 3.94 mg/dL before improving. At discharge, she had complete renal recovery and returned to baseline weight.
Discussion
This patient met criteria for classical SOS with early post-HCT onset, hyperbilirubinemia, weight gain, and ascites. Despite standard therapy with defibrotide and diuretics, she progressed to severe fluid overload and impending dialysis. Given similarities to cirrhotic-HRS, terlipressin was used to improve renal perfusion via splanchnic vasoconstriction. Her rapid clinical improvement supports its potential role in reversing SOS-associated AKI. While approved only for cirrhotic-HRS, this case highlights a possible role in non-cirrhotic vasodilatory states. As dialysis in HCT carries >80% mortality, early reversal is critical. This is the first reported case of successful terlipressin use in SOS-AKI.