Proximal tubular reabsorption was studied by the split drop micropuncture technique in HgCl2-induced severe as well as mild acute renal failure. 4 mg/kg of HgCl2 given subcutaneously to normal rats resulted in severe and usually oliguric acute renale failure at 48 h, mean plasma creatinine and urea having risen to 6.9 +/- 0.4 and 420 +/- 30 mg%. On inspection of the kidney surface, usually more than 50% of the convolutions appeared white opaque and collapased. Split drop reabsorption of 0.9% NaCl, 20% mannitol and 20% albumin was markedly accelerated in these necrotic tubular segments, while reabsorptive rates were usually quite reduced in the normal-looking red transparent convolutions. DOCA/saline-pretreated rats developed mild renal failure, with plasma creatinine and urea rising slightly to 1.6 +/-0.3 and 83 +/- 14 mg%, respectively, at 48 h after 4 mg/kh HgCl2. Reabsorptive rates were almost uniformly reduced from 0.55 +/- 0.02 in controls to 0.32 +/- 0.03 nl-mm-2 sec-1 in mild HgCl2-induced acute renale failure. Mild proximal tubular injury features decreased reabsorptive rate while severely damaged tubules appear to be leaky to the extent of allowing rapid disappearance from the tubular lument of the normally barely reabsorbable 20% albumin. Although compatible with unrestricted passive backflow being an additional factor in the pathogenesis of HgCl2-induced acute renal failure, these results do not challenge the importance of primary filtration failure.