Role of serum levels of intraoperative brain natriuretic peptide for predicting acute kidney injury in living donor liver transplantation.

ABSTRACT

BACKGROUND: Patients with end-stage liver disease frequently experience acute kidney injury (AKI) after living donor liver transplantation (LDLT). Serum levels of brain natriuretic peptide (BNP) have increasingly been accepted as a predictor of AKI in clinical settings. This study investigated the predictive role of intraoperative BNP levels in the early development of AKI after LDLT. PATIENTS AND METHODS: Adult patients (≥19 years old) who had undergone elective LDLT from January 2011 to December 2017 were classified into the non-AKI and AKI groups according to the Kidney Disease Improving Global Outcomes criteria. Serum levels of BNP were measured three times in the preanhepatic, anhepatic, and neohepatic phases. Perioperative data in recipients and donors were analyzed retrospectively. RESULTS: Sixty-one patients (22.4%) suffered from AKI immediately after LDLT. Severity according to AKI stage was as follows 28 patients in stage 1 (10.3%), 18 patients in stage 2 (6.6%), and 15 patients in stage 3 (5.5%). In the neohepatic phase, both BNP levels and proportions of patients with high BNP levels (≥100 pg/mL) were higher in the AKI group than in the non-AKI group. Only BNP levels in the non-AKI and AKI stage 1 groups significantly decreased from the preanhepatic phase to the neohepatic phase; those in AKI stages 2 and 3 groups did not. In particular, BNP levels of all AKI stage 3 patients increased to more than 100 pg/mL, and the proportion of patients with high levels also increased significantly through the surgical phases in the AKI stage 3 group. In multivariate analyses, BNP levels in the neohepatic phase were significantly associated with early development of AKI after LDLT, as well as the total amount of packed red blood cells in transfusions and total duration of graft ischemia. CONCLUSIONS: Monitoring serum levels of BNP is useful for predicting the early development of AKI after LDLT.