BACKGROUND: Diabetic nephropathy is one of the most serious complications of diabetes, and is the leading cause of chronic renal failure. Vascular endothelial growth factor (VEGF) plays an important role in the pathophysiology of diabetic retinopathy, which can be blocked by ACE inhibitors, but its precise role in diabetic nephropathy is uncertain. METHODS: 32 eight week-old Sprague-Dawley male rats were prepared, of which 16 were chosen for injection with streptozotocin (60 mg/kg) into the peritoneal cavity, with the goal of inducing diabetes. One week later, the peripheral blood sugar, taken from the tail vein was checked. A glucose level exceeding 200 mg/dL was taken as evidence of diabetes. The rats were divided into 4 groups of 8. Group I served as a control. Group II was treated with angiotensin II receptor blockade (L-158,809, 5 mg/kg/day, in drinking water). Group III consisted of diabetic rats and group IV diabetic rats treated with the same angiotensin II receptor blockade (L-158,809). At the beginning of the experiment and on 8th and 12th weeks, 24-hour urine protein and body weight checks were performed. At the end of the study, I extracted kidney and the glomerular volumes and optical densities of the VEGF expression in the glomeruli compared. RESULTS: The basal characteristics were initially the same. However, on weeks 8 and 12 the amount of 24-hour urine protein had increased in groups III and IV (p<0.05). By week 12, it was noticeably greater in group III than in group IV (p<0.05). The glomerular volume was also greater in groups III and IV (p<0.05). Optical density of the VEGF in the glomeruli had increased more in group III than in groups I, II and IV (p<0.05). CONCLUSION: VEGF plays a precise role in diabetic nephropathy, and angiotensin II receptor blockade can reduce diabetic nephropathy by suppressing the expression of VEGF.