The current study was designed to examine the hypothesis that exposure of glomerular capillary cells to circulating VEGF or VEGF produced locally in the kidney would modulate endothelial permeability through a noninflammatory mechanism, thus inducing albuminuria. Taken together all the data of this study we were not able to support this hypothesis .We concloude thatVEGF is not the vascular premability factor involved in the pathogenesis on minimal change nephritist. Further, high urinary VEGF levels may merely reflect podocyte loss and urinary podocyte excretion rather than an active involvement of VEGF in the disease process. There is no correlation between glucocorticoid receptors expression by lymphocytes and the plasma or urinary concentrations of VEGF. Meanwhile we were able to prove that the extent of glucocorticoid receptor expression by lymphocytes is inversely related to the time interval from the start of steroid treatment to complete remission. We recommend assessment of the glucocorticoid receptors expression by lymphocytes in patients with nephrotic syndrome to predict the clinical response before starting glucocorticoid therapy in childern.