Abstract
Solid clinical prospective studies investigating the association between hepatic ischemia/reperfusion injury (HIRI) and acute kidney injury (AKI) after liver transplantation are missing. HIRI, reflected by transaminase release, induces AKI in rodents, and retrospective studies suggest a similar association in humans. This prospective cohort study determined risk factors for AKI in 80 adult liver-only recipients. AKI defined by Risk, Injury, Failure, Loss, and End-Stage Kidney Disease (RIFLE) criteria developed in 21 (26%) recipients at 12 hours after reperfusion (interquartile range, 6 hours to postoperative day [POD] 1); 13 progressed from "risk" to "injury"; 5 progressed to "failure." In AKI patients, creatinine (Cr) increased during liver transplantation and was higher versus baseline at 6 hours to POD 4, whereas perioperative Cr remained stable in those without AKI. Plasma heart-type fatty acid-binding protein was higher 12 hours after reperfusion in AKI patients, though urinary kidney injury molecule 1 and neutrophil gelatinase-associated lipocalin were similar between those with or without AKI. Peak aspartate aminotransferase (AST), occurring at 6 hours, was the only independent risk factor for AKI (adjusted odds ratio, 2.42; 95% confidence interval, 1.24-4.91). Early allograft dysfunction occurred more frequently in AKI patients, and intensive care and hospital stays were longer. Patient survival at 1 year was 90% in those with AKI versus 98% in those without AKI. Chronic kidney disease stage ≥ 2 at 1 year was more frequent in patients who had had AKI (89% versus 58%, respectively). In conclusion, AKI is initiated early after liver reperfusion and its association with peak AST suggests HIRI as a determinant. Identifying operating mechanisms is critical to target interventions and to reduce associated morbidity. Liver Transplantation 23 634-644 2017 AASLD.