Predictive Role of the D-Dimer Level in Acute Kidney Injury in Living Donor Liver Transplantation: A Retrospective Observational Cohort Study

This study aimed to determine the association between serum D-dimer levels and the risk of acute kidney injury (AKI) in patients undergoing living donor liver transplantation (LDLT). Clinical data of 675 patients undergoing LDLT were retrospectively analyzed. The exclusion criteria included a history of kidney dysfunction, emergency cases, and missing data. The final study population of 617 patients was divided into the normal and high D-dimer groups (cutoff: 0.5 mg/L). After LDLT, 145 patients (23.5%) developed AKI. A high D-dimer level (>0.5 mg/L) was an independent predictor of postoperative development of AKI in the multivariate analysis when combined with diabetes mellitus [DM], platelet count, and hourly urine output. AKI was significantly higher in the high D-dimer group than in the normal D-dimer group (odds ratio [OR], 2.792; 95% confidence interval [CI], 1.227–6.353). Patients with a high D-dimer exhibited a higher incidence of early allograft dysfunction, longer intensive care unit stay, and a higher mortality rate. These results could improve the risk stratification of postoperative AKI development by encouraging the determination of preoperative D-dimer levels in patients undergoing LDLT.

Predicting the Recurrence of Hepatocellular Carcinoma after Primary Living Donor Liver Transplantation Using Metabolic Parameters Obtained from 18F-FDG PET/CT

This study evaluated the prognostic value of metabolic parameters based on the standardized uptake value (SUV) normalized by total body weight (bwSUV) and by lean body mass (SUL) measured on 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) for predicting tumor recurrence after primary living donor liver transplantation (LDLT) in patients with hepatocellular carcinoma (HCC) without transplantation locoregional therapy. This retrospective study enrolled 49 patients with HCC. The maximum tumor bwSUV (T-bwSUVmax) and SUL (T-SULmax) were measured on PET. The maximum bwSUV (L-bwSUVmax), mean bwSUV (L-bwSUVmean), maximum SUL (L-SULmax), and mean SUL (L-SULmean) were measured in the liver. All metabolic parameters were evaluated using survival analyses and compared to clinicopathological factors. Tumor recurrence occurred in 16/49 patients. Kaplan–Meier analysis revealed that all metabolic parameters were significant (p < 0.05). Univariate analysis revealed that prothrombin-induced by vitamin K absence or antagonist-II; T-stage; tumor number; tumor size; microvascular invasion; the Milan criteria, University of California, San Francisco (UCSF), and up-to-seven criteria; T-bwSUVmax/L-bwSUVmean; T-SULmax; T-SULmax/L-SULmax; and T-SULmax/L-SULmean were significant predictors. Multivariate analysis revealed that the T-SULmax/L-SULmean (hazard ratio = 115.6; p = 0.001; cut-off, 1.81) and UCSF criteria (hazard ratio = 172.1; p = 0.010) were independent predictors of tumor recurrence. SUL-based metabolic parameters, especially T-SULmax/L-SULmean, were significant, independent predictors of HCC recurrence post-LDLT.

A Mortality Case Caused by Thrombotic Microangiopathy after Successful Bloodless Living Donor Liver Transplantation

Thrombotic microangiopathy (TMA) after solid organ transplantation is infrequent and its etiology remains still unclear. Nevertheless, if early diagnosis and early therapies are not performed, it can lead to severe life-threatening complications and even death. A 54-year-old female (a Jehovah’s Witness) was diagnosed with drug-induced toxic hepatitis and was decided to undergo bloodless living donor liver transplantation (LDLT). After the successful LDLT, the patient’s condition deteriorated, and she was diagnosed with TMA during further evaluation. We tried to proceed with plasma exchange-based treatment, but she and her family declined according to their religious beliefs. The patient expired 4 days after the diagnosis. Physicians should maintain a high level of suspicion for TMA after liver transplantation when clinical manifestations are observed.