Trial reportHepatology (Baltimore, Md.)2026
The relationship between mean arterial pressure and terlipressin in hepatorenal syndrome-acute kidney injury reversal: A post hoc analysis.
Trial report in Hepatology (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- KASL clinical practice guidelines for liver cirrhosis: Ascites and related complications 2026.Clinical and molecular hepatology · 2026Article
- Beyond the Tipping Point: Advances in the Diagnosis and Management of Acute-on-Chronic Liver Failure and End-Stage Liver Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Embracing Imperfect Tools to Decode AKI in Decompensated Cirrhosis.Digestive diseases and sciences · 2026Article
- Treating Hepatorenal Syndrome in the Current Era.Journal of the American Society of Nephrology : JASN · 2026Review
- Use of Terlipressin in Liver Transplant Candidates.Gastroenterology & hepatology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
BACKGROUND AND
aimsTerlipressin reverses hepatorenal syndrome-acute kidney injury (HRS-AKI) by increasing mean arterial pressure (MAP). To further characterize the relationship between terlipressin and MAP and their impact on HRS-AKI reversal, we used patient-level data from phase 3 clinical trials REVERSE and CONFIRM. APPROACH AND
resultsIn this post hoc analysis we employed a linear mixed-effects model to assess terlipressin's impact on MAP, exploring the relationship between MAP, treatment group, and time, incorporating a random intercept for individual patients. Time-dependent Cox models analyzed MAP's role in HRS-AKI reversal. We conducted a mediation analysis to evaluate how time-weighted MAP mediated HRS-AKI reversal. This analysis included 487 patients (60% terlipressin, 40% placebo). At baseline, there were no differences in median MAP between terlipressin and placebo (77 mm Hg vs. 76 mm Hg, p =0.3); the terlipressin group had significantly higher MAPs after randomization (day 1: 85 mm Hg vs. 75 mm Hg; day 3: 81 mm Hg vs. 76 mm Hg; all: p <0.001). In mixed-effects models, terlipressin was associated with a 6.0 mm Hg increase in MAP over placebo occurring on day 1, with no significant interaction between the treatment group and time ( p >0.05). In time-dependent Cox models, each 5 mm Hg increase in MAP was associated with 1.17× the hazard of HRS-AKI reversal (95% CI: 1.11-1.22). In mediation analysis, MAP significantly mediated HRS-AKI reversal, regardless of treatment group (average proportion mediated: 33%, 95% CI: 14-76).
conclusionsThese data highlight that terlipressin leads to an early, sustained increase in MAP, which is a key pharmacodynamic target for HRS-AKI reversal.
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