Diabetic nephropathy is a serious complication of diabetes mellitus affecting 25-40% of patients with type 1 or type 2 diabetes within 20-25 years of the onset of the disease. However, the great majority of patients are those with type 2 diabetes. In this condition, the earliest clinical evidence of nephropathy is the appearance of low but abnormal levels of albumin in the urine. This stage is referred as microalbuminuria and patients with microalbuminuria are referred to as having incipient nephropathy. As the disease progress, patients reach to macroalbuminuria and, finally, end stage renal disease. About one third of patients with diabetic nephropathy progress to end stage renal disease. In addition, patients with diabetic nephropathy generally develop systemic hypertension. Several agents are used to delay the progression of diabetic nephropathy include beta blockers, calcium channel blockers, diuretics, angiotensin converting enzyme (ACE) inhibitors, and angiotensin II receptor antagonists (AIIRAs).
The exact cause of diabetic nephropathy is unknown, but several mechanisms have been postulated. Hyperglycemia increases the expression of transforming growth factor-beta (TGF-beta) in the glomeruli and of matrix proteins specifically stimulated by this cytokine. TGF-beta may contribute to both the cellular hypertrophy and enhanced collagen synthesis observed in persons with diabetic nephropathy. Also, hyperglycemia may activate protein kinase C, which may contribute to renal disease and other vascular complications of diabetes.