ABSTRACT
Diabetic nephropathy is characterized by the enlargement of glomerular mesangium because of the accumulation of extracellular matrix proteins, and is a leading cause of end-stage renal disease (1,2). Clinical studies in subjects with type 1 and type 2 diabetes clearly link hyperglycemia to vascular complications, including diabetic nephropathy (3,4). Hyperglycemia is responsible for the development and progression of diabetic nephropathy through metabolic derangements, including increased oxidative stress, renal polyol formation, activation of protein kinase C-mitogen-activated protein kinases, and accumulation of advanced glycation end products, as well as such hemodynamic factors as systemic hypertension and increased intraglomerular pressure (5). However, the definite mechanism of mesangial cell activation by high ambient glucose has not been investigated.
