Terlipressin Can Serve as an Effective Bridge to Transplant in Pediatric HRS-AKI, Suggests Study

HRS-AKI develops in approximately 5–10% of children with chronic liver disease. The condition arises from complex circulatory changes linked to portal hypertension. Marked splanchnic vasodilation leads to reduced mean arterial pressure, triggering compensatory renal vasoconstriction. The resulting fall in renal perfusion causes functional kidney failure. Episodes may be precipitated by sepsis or systemic inflammation and can be further complicated by cirrhotic cardiomyopathy.

Liver transplantation remains the only definitive treatment for HRS-AKI. However, accumulating evidence—largely derived from adult randomized trials—indicates that terlipressin, administered with albumin, can reverse renal dysfunction in many cases. Although paediatric data are limited, early studies suggest that terlipressin may also be effective in children, potentially stabilizing renal function and serving as a bridge to transplantation. Importantly, limited long-term observations indicate that renal recovery after transplant is achievable in some children.

The authors emphasize that careful patient selection is critical. Terlipressin should be initiated at low doses and titrated gradually, with close monitoring for adverse effects. Contraindications, extrapolated mainly from adult experience, include severe liver or renal failure and heightened risk of pulmonary oedema. In children, additional considerations such as vascular access challenges and the risk of drug extravasation must be taken into account.

Despite its potential, the evidence base in paediatrics remains sparse. Most current clinical guidance relies heavily on adult data, although the causes and clinical course of chronic liver disease differ between children and adults. The authors call for coordinated international collaboration to better characterize both short- and long-term outcomes in this population, including the risk of chronic kidney disease before and after transplantation.

The review also highlights the importance of biomarker research. In adults with cirrhosis and AKI, urinary neutrophil gelatinase-associated lipocalin (uNGAL) has been shown to help predict response to terlipressin therapy. If validated in children, such biomarkers could aid in risk stratification and treatment decisions. Serum cystatin C has also shown promise as a sensitive marker of renal dysfunction in paediatric transplant recipients, though its role in HRS-AKI specifically requires further investigation.

Overall, the authors conclude that while liver transplantation remains central to management, terlipressin offers a valuable therapeutic option in carefully selected children with HRS-AKI. Expanding collaborative research efforts and integrating biomarker-driven approaches may help refine treatment strategies and improve outcomes in this high-risk group.