Nephron function in postischemic acute renal failure.

Acute renal failure was induced in rats by clamping the renal artery for 45 min. After reestablishing renal blood flow, tubular heterogeneity was observed, with (1) seemingly normal tubules, (2) dilated tubules and (3) collapsed tubules. Micropuncture techniques were used to examine the hydrostatic pressures in the different nephrons and superficial vessels, and also to determine single nephron glomerular filtration rate. The dilated tubules showed minimal filtration, due to an elevated intratubular pressure probably caused by obstructions; in these nephrons filtration could be induced by lowering the intratubular pressure. In the "normal" nephrons there was some filtration, as the proximal tubular pressure was only moderately increased. No filtration took place in the collapsed type, probably as a result of glomerular ischemia and consequently decreased glomerular capillary pressure. The kidneys also exhibited isosthenuric polyuria with a reduced potassium secretion. It is suggested that a medullary ischemia will lead to interstitial and intracellular edema and eventually cell necrosis with subsequent formation of obstructions in the loops of Henle. The obstructions would explain the increase in proximal tubular pressure and the decrease in total kidney filtration to about 5% of the normal. It is proposed that the deficient urine concentration ability and the inhibited potassium secretion are caused by the ischemic damage to the renal medulla.