“…Such procoagulant activity is substantiated by the presence of shortened platelet half life, blood hypercoagulability and hyperviscosity due to overcompensatory production, fibrin or traced element of fibrin, elevated fibrin degradation product in the serum and urine [1]. However, the ability of the glomerular endothelium to release an adequate amount of vasodilators, delineated by the mean of the intrarenal hemodynamic study (renal plasma flow 704 B 102 ml/min; control 600 ml/ min/1.73 m 2 ), is well maintained in this mild category of nephrosis [2]. The degree of glomerular endothelial dysfunction is amplified in other forms of nephrosis with greater clinical severity.…”