Hepatic ischemia/reperfusion injury associates with acute kidney injury in liver transplantation: Prospective cohort study

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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.

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