About 20-40% of type 2 diabetic patients may develop diabetic nephropathy (DN) as its complication. The pathogenesis of DN is a complex one. Classically, metabolic and hemodynamic impairment are considered as its pathogenesis. This view has evolved tremendously in recent years. Large number of evidences points that inflammation is a key event in the development and progression of DN. Among several inflammatory molecules, proinflammatory cytokines such as interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α) are known to be involved. Chronic condition of hyperglycemia responsible for the formation of proinflammatory cytokines via advanced glycation end products (AGE) pathway and protein kinase C (PKC) pathway. These proinflammatory cytokines exert signaling pathway that lead to extracellular matrix (ECM) accumulation, glomerular basement membrant (GBM) thickening, and glomerulosclerosis, ultimately lead to development and progression of diabetic nephropathy. Knowing this mechanism in detail beneficial for future treatment. Intervention in these signaling pathway may benefit to development of novel therapeutic approach.
