Hyperleptinemia Is a Risk Factor for the Development of Central Arterial Stiffness in Kidney Transplant Patients

Abstract

BackgroundArterial stiffness could cause adverse outcomes in kidney transplant (KT) patients. Leptin has a role in influencing vascular smooth muscle that may contribute to atherosclerosis. The aim of this study was to evaluate the relationship between fasting serum leptin concentration and carotid-femoral pulse wave velocity (cfPWV) in KT patients. Materials and MethodsFasting blood samples were obtained from 55 KT patients and 65 subjects from the outpatient department were enrolled as the control group. The cfPWV values of >10 m/s were used to define as the high arterial stiffness group and <10 m/s as the low arterial stiffness group. The predictive ability of leptin for arterial stiffness of KT was assessed using receiver operating characteristic (ROC) curve and multivariate logistic regression analyses. ResultsKidney transplant patients had lower hemoglobin, but higher blood urea nitrogen, creatinine, total cholesterol, diastolic blood pressure, intact parathyroid hormone levels, and leptin levels than controls. Although cfPWV levels were higher in KT patients, there is no difference of cfPWV levels between KT patients and control (P = .595). Fifteen KT patients (27.3%) were defined in the high arterial stiffness group, and serum leptin level was higher in the high arterial stiffness group compared with the low arterial stiffness group in KT patients (P < .001). Multivariate logistic regression analysis showed that leptin (odds ratio: 1.044, 95% confidence interval [CI]: 1.016–1.072, P = .002) was an independent predictor of arterial stiffness in KT patients. The sensitivity, specificity, positive predictive value, negative predictive value, and area under the ROC curve predicting arterial stiffness in KT patients were 73.33%, 87.5%, 68.7%, 89.7%, and 0.828 (95% CI: 0.703–0.917, P < .001), and the leptin cut-off value was 74.14 ng/mL. ConclusionSerum fasting leptin level could predict the development of central arterial stiffness of KT patients.