In the present study, the pathophysiologic role of glomerular hemodynamic factors in the early phase of HgCl2-induced acute renal failure is evaluated in the dog. This model of moderate ARF is characterized by a parallel fall in glomerular filtration rate (ΔGFR, -43%) and renal blood flow (ΔRBF, -38%) within the first three hours after HgCl2administration. Glomerular hemodynamics were studied by analysis of PVP-sieving curves. There was a significant shift of these curves upward and to the right during the 3 hours that followed the injection of HgCl2. From this analysis, no arguments for tubular back-leak could be found. Mathematical analysis of the curves revealed a fall in effective filtration pressure (EFP) in presence of an unchanged glomerular ultrafiltration coefficient (Kf) (ΔEFP, -40±4%; p<0.01; AKf, +5± 1%; p>0.05 vs. control). No major changes occurred in glomerular colloid osmotic pressure. Subsequently, the early fall of GFR in this toxic model of acute renal failure was essentially attributed to a decrease of effective filtration pressure due to either tubular obstruction and/or mainly to renal hemodynamic changes.