Concentrating Mechanism and Histology During the Course of Unilateral Acute Renal Failure in the Dog

Abstract

Unilateral acute renal failure was induced in dogs by a one hour clamping of the renal pedicle followed by an intravenous injection of acid hematin. The contralateral kidney remained largely unaffected and served as a control. The animals were then divided in four groups and studied at 2, 7, 12 and 21 days after the initial procedure. A diminished urine flow, urinary concentration and urea excretion were found in the damaged kidney, along with a decreased medullary content of sodium and urea, an increased medullary tissue water and histologic alterations. Concentrating capacity and tissue sodium and urea content were still reduced at the 12th day but were largely recovered after 21 days. Numerous distal intratubular casts, proximal tubular collapse and degeneration of proximal and distal convolutions and ascending loops of Henle were predominant at 48 h, followed later by progressive proximal and distal tubular dilatation and a decreasing number of casts. At 21 days the histologic picture was almost normal. The findings show that the urinary concentrating defect is mainly a consequence of a decreased medullary content of sodium and urea. Histologically evident damage to the ascending limb of Henle suggests that an impaired sodium transport at this level could be partly responsible for the decreased medullary sodium content. Other mechanisms contributing significantly to the medullary depletion of sodium and urea could be a primary fall in GFR and/or a massive backdiffusion of filtrate at the proximal tubules.