Type-2 Diabetic Nephropathy: A Proinflammatory Cytokine Associated Disease due to Hyperglycemia Induced Oxidative Stress -

Diabetic nephropathy is one of the major complications of type-2 diabetes and it is currently the leading cause of end-stage renal disease. Hyperglycemia is the driving force for the development of diabetic nephropathy; it increases the production of free radicals resulting in oxidative stress. Renal tissue macrophages, T cells, and neutrophils produce various reactive oxygen species, proinflammatory cytokines (tumor necrosis factor (TNF-α) and interleukin (IL-6)} and various growth factors in renal cells of long term standing type2 diabetes, which modulate the local response and increases the inflammation within the diabetic kidney. Previously, diabetes was not thought to be an immune disease; however, there is increasing evidence supporting a role for inflammation in type-2 diabetes. Inflammatory cells, cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and cell adhesion molecules (CAMs) have all been implicated in the pathogenesis of diabetic nephropathy via increased vascular inflammation and fibrosis. The study aimed to predict the development of diabetic nephropathy in type-2 diabetes due to oxidative stress.