Oxidative stress is increased in diabetes and the overproduction of the ROS (full form ?) in diabetes is a direct consequence of persistent hyperglycemia for the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α and interleukin (IL-6) in renal cells, which are the factors responsible for diabetic complications i.e. diabetic nephropathy. The study aimed to predict the development of type 2 diabetic nephropathy due to persistent hyperglycemia induced oxidative stress producing inflammation. Serum levels of inflammatory markers (IL-6 and Tnf-α), antioxidants, [Glutathione reductase (GR) and Glutathione peroxidase (GPx)], plasma malondialdehyde (MDA), fasting blood sugar, urea and creatinine levels were estimated in controls (n=50), controlled diabetes without diabetic nephropathy, T2DM without microvascular complication (n=50, groupI) and T2DM with diabetic nephropathy (n=100, group II). Sample was collected from J.A group of hospitals, GRMC, Gwalior (M.P) and ethical committee has approved this research work. Statistical method was done by using one way Anova utlizing Dunnet T3 test. Serum levels of inflammatory markers (IL-6 and Tnf-α), malondialdehyde, fasting blood sugar, were high in group II as compared to both group I and controls, (P<0.001), with group II having more significant than group I (P<0. 001). Antioxidant enzyme glutathione peroxidase was found to be decreased in both groups of diabetic patients as compared to controls, (P<<0.05), with group II showing significant than group I at (P<0.001). Glutathione reductase was found to be normal range in all the groups. Serum urea and creatinine levels were increased in group II, (P<0.001), but serum levels were within normal range in group I and healthy controls. Results of the present study indicates that inflammatory markers and oxidative stress are increased with decreased antioxidant defense levels in patients with diabetic nephropathy due to hyperglycemia induced oxidative stress.