Low serum-free oxygen radicals defense level is associated with peripheral arterial stiffness in kidney transplantation patients

Oxidative stress is a causative mechanism of vascular alterations resulting in arterial stiffness. The aim of this study was to evaluate the relationship between oxidative stress and arterial stiffness among kidney transplantation (KT) patients. Fasting blood samples were obtained from 70 KT patients. Arterial stiffness was measured by brachial-ankle pulse wave velocity. Oxidative stress was measured by free oxygen radicals testing (FORT) and free oxygen radicals defense (FORD). We found that diabetes (P = 0.005), hypertension (P = 0.001), metabolic syndrome (P = 0.029), age (P = 0.007), KT duration (P = 0.007), waist circumference (P = 0.039), systolic blood pressure (P < 0.001), diastolic blood pressure (P = 0.004), pulse pressure (P = 0.001), triglycerides (P = 0.049), fasting glucose (P = 0.003), insulin (P = 0.011), homeostasis model assessment of insulin resistance (HOMA-IR, P = 0.002), and FORT (P = 0.014) were all higher in the high arterial stiffness group, while HDL-C (P = 0.004) and FORD (P = 0.009) were lower. Multivariate logistic regression analysis of all significant variables showed that FORD level (OR: 0.849, 95% CI: 0.740-0.973, P = 0.019) is inversely associated with arterial stiffness. Logarithmically transformed HOMAIR (β = -0.280, P = 0.019) was independently associated with FORD levels in KT patients. Our study showed that KT patients with higher serum FORT level and lower FORD level had high arterial stiffness. Low serum FORD level is an independent predictor of peripheral arterial stiffness in KT patients. Among these KT patients, logarithmically transformed HOMA-IR is negatively associated with serum FORD level.