Abstract
It is well known that patients with acute renal failure have urinary concentrating defect even after clinical recovery. However, few attemps were made to study the mechanisms responsible for the defect and its improvement in acute renal failure. In the present work, urinary concentrating ability and intrarenal hemodynamics were studied in acute renal failure in previously uni-nephrectomized rabbits, caused by 2-hr clamping of the contralateral renal artery. Arterial clamping resulted in acute oliguric renal failure comparable to that in man. Directly meas-ured renal blood flow restored fairly well immediately after release of clamping. Superficial cortical blood perfusion, estimated by an isotope-labelled microsphere technique, was slightly reduced for the first several days following the occlusion, whereas deep cortical perfusion increased. During the oliguric stage, medu-llary osmolality was markedly diminished, concomittently with reduced (U/P) osm. CIN, EPAH and fractional sodium reabsorption were tremendously decreased. Light microscopic observations revealed tubular necrosis and intratubular cast formation. During the early diuretic stage, which uniformly followed the oliguric stage, CIN, medullary osmola-lity and (U/P)osm were reduced. Intratubular casts disappeared while regenerated tubular cells were focally observed. In 2 weeks after the occlusion, fairly well improved CIN, EPAH, sodium reabsorption, medullary osmolality and (U/P)osm, and a remarkable regeneration of tubular epithelium were found. In 7 weeks, CIN and EPAH returned to the preclamping values whereas medullary osmolality decreased again with an appearance of medullary fibrosis. Also, (U/P)osm did not completely restore. The findings indicate that urinary concentrating ability restores slowly as compared with other renal functions in ischemic acute renal failure of rabbits.
