Diabetes is a chronic metabolic disorder that continues to present as a major health problem worldwide. It is the\nmajor cause of chronic kidney disease which in turn may lead to end-stage renal disease (ESRD) ending up in dialysis. Diabetic\nnephropathy (DN) is characterized by the development of overt proteinuria, increasing systemic blood pressure and declining\nrenal function. Various risk factors are involved in the development and progression of DN, among them hyperglycemia and\narterial hypertension are the major contributor. Hyperglycemia induced metabolic and hemodynamic pathways are proven to\nbe the mediators of kidney disease. Hyperglycemia causes the formation of Amadori products, which are the altered proteins\nand advanced glycation end products (AGE) are the molecular players in the phases of DN. Hemodynamic changes, hypertrophy,\nextracellular matrix accumulation, growth factor/cytokine induction, ROS formation, podocyte damage, proteinuria and\ninterstitial inflammation are the steps in the advancement of DN. Recent studies examining the pathogenesis of diabetic\ncomplications have focused on the complex interaction between genetic and hemodynamic mechanisms in addition to metabolic\nfactors such as advanced glycation, protein kinase C (PKC) activation and polyol production. The importance of the various\ncomponents, particularly with regard to the progression of DN, is currently being explored with the assistance of targeted drug\nintervention studies.
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