Background: Vascular endothelial growth factor (VEGF) increases endothelial permeability. VEGF is produced in podocytes and functional receptors are located on endothelial glomerular cells. The aim of the current study in diabetic patients with normal renal function to various degrees of proteinuric nephropathy was therefore to unravel a possible role of the most important isoform VEGF(165) for albuminuria and to investigate the impact of therapy with an inhibitor of the renin-angiotensin system on VEGF(165) secretion.
Subjects and methods: A cross-sectional study in 72 patients (41 female, 31 male) with long-standing type 1 (n = 35, mean age 43.3 years, range 22-67) or type 2 (n = 37, mean age 66 years, range 53-83) diabetes mellitus was performed; in 19 patients the serum creatinine value was >1.5 mg/dl. Twenty-six healthy volunteers (17 female, 9 male, mean age 34.8 years, range 19-58) with normal renal function served as controls. Serum and urinary VEGF(165) was measured by ELISA. Urinary albumin was measured nephelometrically. Mann Whitney U tests were used for comparisons.
Results: In type 1 and type 2 diabetics mean urinary VEGF(165) concentration amounted to 112 +/- 88 (mean +/- SD) and 88 +/- 85 ng/l, respectively, compared to 101 +/- 60 ng/l in the normal volunteers (NS vs. diabetics). The respective mean urinary albumin concentrations were 443 +/- 1029, 394 +/- 749 and 20 +/- 33 mg/l (p < 0.01 vs. diabetics type 2). There was a correlation between urinary VEGF and albumin, but only in patients with type 2 diabetes (R = 0.497; n = 36; p = 0.002). Urinary VEGF(165) was similar in patients with (n = 40) and without ACE inhibitor/AT1 antagonist therapy (n = 32) and in normal volunteers, whereas serum VEGF(165) was higher in the treated type 1 diabetics.
Conclusions: These results may suggest that VEGF(165) plays some role in the development of albuminuria in diabetic nephropathy due to type 2 but not type 1 diabetes.
Copyright 2003 S. Karger AG, Basel