Glomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure.

Complete occlusion of the left renal artery for 60 min in the rat produced anuric acute renal failure after 1 day. Using fluorescence microscopy, a television system combined with double slit densitometry, and micropuncture techniques, tubular pressure and tubular flow rates were determined in different segments of superficial nephrons. Intratubular pressures in proximal convolutions of the postischemic kidney were largely heterogeneous due to abnormally increased flow resistance in proximal tubules which were filled with loose obstructive material. Proximal tubular pressure in the control kidney was independent of the site of its measurement and had a mean value of 14.1 mm Hg. In the postischemic kidney pressure decreased gradually along the proximal tubule, its value in the early and late segments being 16.3 and 9.7 mm Hg, respectively. Low pressure in late proximal convolutions excludes a significant flow impediment due to obstruction in more distal segments. The mean nephron filtration rate (SNGFR) obtained by extrapolation of tubular flow data was 62% of the control value, whereas tubular reabsorption was estimated to be 50% above normal. Reduced SNGFR and increased outflux caused a total reabsorption of tubular fluid within 60% of proximal convoluted tubule length. The partial reduction of SNGFR can be explained by increased pressure in early proximal convolutions and reduced glomerular plasma flow known for these kidneys, without postulating a change in glomerular permeability. Tubular obstruction and increased passive outflux in proximal tubules due to cellular damage appear to be crucial mechanisms responsible for the loss of renal function in this model of acute renal failure.