Acute renal failure (ARF) in low-flow states may be reversed by increasing renal perfusion. When hemodynamics are maximized, renal perfusion can only be improved by shunting a higher proportion of cardiac output to the kidney; however, in low-flow states, this reduces already compromised systemic pressure and perfusion to other organs. Increasing perfusion using venous blood (VB) would be an attractive option because decreased systemic pressure and perfusion to other organs could be avoided. However, it is not known whether VB can provide adequate oxygen delivery to restore or maintain renal function. We studied whether antegrade VB perfusion of the kidney via the renal artery would restore urine output (UO) and glomerular filtration rate (GFR) in hypoperfused ARF. Shock was induced in six dogs via a hemorrhagic protocol resulting in a systolic blood pressure of 50-70 mm Hg, a mixed venous oxygen saturation of 25% to 40%, and a UO <10% of baseline. After 60 mins of shock, the left renal artery was cannulated under fluoroscopy and perfused at pressures of 100-150 mm Hg for 30 mins with VB drawn from the vena cava and delivered by an extracorporeal pump system. The right kidneys were controls and remained hypoperfused. All VB-perfused kidneys recovered renal function after a sustained period of shock and marked oliguria: UO from 0.7 +/- 1.6 mL/hr to 101 +/- 58 mL/hr (p <.01); GFR from approximately 0 to 70.3 +/- 55 mL/min (p =.04). The control kidneys' UO (0.7 +/- 1.6 mL/hr) and GFR (0 mL/min) remained unchanged throughout the study. The experimental kidneys were able to extract oxygen from VB (O2 saturation, 31 +/- 7% to 16 +/- 4%; p =.01). When flow is controlled, kidneys in hypoperfused ARF can extract sufficient oxygen from antegrade VB perfusion to restore renal function (UO and GFR).