New-onset hyperglycemia immediately after liver transplantation: A national survey from China Liver Transplant Registry.

BACKGROUND: New-onset hyperglycemia (NOH) is a common phenomenon after liver transplantation (LT), but its impact on clinical outcomes has not yet been fully assessed. We aimed to evaluate the etiology and prognosis of NOH within 1 month after LT. METHODS: The data of 3339 adult patients who underwent primary LT from donation after citizen death between January 2010 and June 2016 were extracted from China Liver Transplant Registry database and analyzed. NOH was defined as fasting blood glucose ≥7.0 mmol/L confirmed on at least two occasions within the first post-transplant month with or without hypoglycemic agent. RESULTS: Of 3339 liver recipients, 1416 (42.4%) developed NOH. Recipients with NOH had higher incidence of post-transplant complications such as graft and kidney failure, infection, biliary stricture, cholangitis, and tumor recurrence in a glucose concentration-dependent manner as compared to non-NOH recipients (P < 0.05). The independent risk factors of NOH were donor warm ischemic time >10 min, cold ischemic time >10 h, anhepatic time >60 min, recipient model for end-stage liver disease score >30, moderate ascites and corticosteroid usage (P < 0.05). Liver enzymes (alanine aminotransferase and gamma-glutamyltranspeptidase) on post-transplant day 7 significantly correlated with NOH (P < 0.001). CONCLUSIONS: NOH leads to increased morbidity and mortality in liver recipients. Close surveillance and tight control of blood glucose are desiderated immediately following LT particularly in those with delayed graft function and receiving corticosteroid. Strategic targeting graft ischemic injury may help maintain glucose homeostasis.

Major influence of renal function on hyperlipidemia after living donor liver transplantation.

AIM: To investigate the impact of renal and graft function on post-transplant hyperlipidemia (PTHL) in living donor liver transplantation (LDLT). METHODS: A total of 115 adult patients undergoing LDLT from January 2007 to May 2009 at a single center were enrolled. Data were collected and analyzed by the China Liver Transplant Registry retrospectively. PTHL was defined as serum triglycerides ≥ 150 mg/dL or serum cholesterol ≥ 200 mg/dL or the need for pharmacologic treatment at the sixth month after LDLT. Early renal dysfunction (ERD) was defined as serum creatinine ≥ 2 mg/dL and/or the need for renal replacement therapy in the first post-transplant week. RESULTS: In 115 eligible patients, the incidence of PTHL was 24.3%. Recipients with PTHL showed a higher incidence of post-transplant cardiovascular events compared to those without PTHL (17.9% vs 4.6%, P = 0.037). Serum creatinine showed significant positive correlations with total serum triglycerides, both at post-transplant month 1 and 3 (P < 0.01). Patients with ERD had much higher pre-transplant serum creatinine levels (P < 0.001) and longer duration of pre-transplant renal insufficiency (P < 0.001) than those without ERD. Pre-transplant serum creatinine, graft-to-recipient weight ratio, graft volume/standard liver volume ratio, body mass index (BMI) and ERD were identified as risk factors for PTHL by univariate analysis. Furthermore, ERD [odds ratio (OR) = 9.593, P < 0.001] and BMI (OR = 6.358, P = 0.002) were identified as independent risk factors for PTHL by multivariate analysis. CONCLUSION: Renal function is closely associated with the development of PTHL in LDLT. Post-transplant renal dysfunction, which mainly results from pre-transplant renal insufficiency, contributes to PTHL.