The vascular basis for acute renal failure in the rat. Preglomerular and postglomerular vasoconstriction

Myohemoglobinuric acute renal failure (ARF) was induced in dehydrated, salt-deficient, salt-loaded, and untreated rats by intramuscular injection of glycerol, and the renal vasculature was studied after 24 hours. Kidneys were prepared for examination by rapid freezing in vivo to -160 degrees C and freeze substitution in -80 degrees C alcohol, and by perfusion fixation with 1% glutaraldehyde in Ringer's solution at 120 mm Hg. Frozen kidneys were examined by light microscopy after paraffin and epoxy resin embedding. Techniques used in examining the perfusion-fixed kidneys were: (1) vascular injection with silicone rubber and clearing in glycerol, (2) electron microscopy, and (3) morphometric evaluation of lumen to wall area ratios of glomerular arterioles. Kidneys of all rats with ARF showed renal cortical arterial and glomerular arteriolar (afferent and efferent) vasoconstriction. The degree of constriction, estimated by lumen to wall ratios, correlated with the degree of azotemia (r = -0.71; P less than 0.001). Differences between all ARF groups and respective controls were highly significant (P less than 0.001). Vasoconstriction was maximal in the dehydrated group, intermediate in the untreated and Na-deficient rats, and lowest in the salt-loaded animals. Glomerular and peritubular capillaries were patent and free of endothelial swelling or thrombi. Glomerular basement membranes and epithelial foot processes showed no morphological alterations. The observations suggest that marked pre- and postglomerular vasoconstriction occurs in established myohemoglobinuric ARF, that it is related to azotemia, and that mechanical vascular obstruction does not play a major role in this experimental model.