DNA fragmentation damage as a predictive marker for diabetic nephropathy in Type II diabetes mellitus

Abstract

Background: Increased production of free radicals and oxidative stress in type II diabetic patients could be one of the probable causes for development of complications. The authors hypothesise that such a mechanism also contributes to the development of diabetic nephropathy in those patients. Aim: The aim of this study was to evaluate the association of DNA fragmentation damage with diabetic nephropathy in type II diabetes mellitus, so as to use it as a future novel predictive marker. Patients and methods: The study population included 100 patients with diabetic nephropathy, 100 diabetic patients without nephropathy and 100 healthy volunteers as controls. Lipid profile, fasting and post-prandial blood glucose, micro-albuminuria (micro-alb) and glycosylated haemoglobin (HbA1c) were assessed in patients and controls. The technique of capillary electrophoresis was used to detect DNA damage. Results: The frequency of DNA damage in peripheral blood mononuclear cells was 71% in diabetic nephropathy compared with 45% in non-nephropathy patients (p < 0.001). None of healthy controls showed such a finding. Oxidative DNA fragmentation in the diabetic nephropathy group was 3.06 times that in the non-nephropathy group. Neither poor glycaemic control nor dyslipidaemia contributed to DNA damage in diabetic patients. Multivariate analysis showed that positive oxidative DNA damage test (OR1.58, p = 0.02) and the duration of ongoing DM (OR 1.48, p = 0.004) were the only independent factors contributing to the occurrence of diabetic nephropathy. Conclusion: Type II diabetic patients have more liability to oxidative DNA damage in general with a significantly higher frequency in diabetic nephropathy. DNA fragmentation analysis can be used as a predictive diagnostic biomarker for diabetic nephropathy.