URINARY ANGIOTENSIN I-CONVERTING ENZYME-ACTIVITY IS INCREASED IN EXPERIMENTAL ACUTE-RENAL-FAILURE

The angiotensin I-converting enzyme (ACE) activity was studied in 2 ex perimental models of acute renal failure: (a) rats treated with a sing le injection of mercuric chloride (1.5 mg/kg) and (b) rats treated wit h a single injection of potassium dichromate (15 mg/kg). Rats were sac rificed 24 and 48 h after mercuric chloride or potassium dichromate in jection. ACE activity was measured in urine, serum, and kidney. These data were compared with vehicle-treated rats. Rats with acute renal fa ilure had proteinuria, polyuria, and decreased creatinine clearance. T he damage to the kidney proximal tubule was evident by (a) the histolo gical analysis at light and electron microscopy, (b) the augmentation in the urinary excretion of dipeptidyl aminopeptidase IV and N-acetyl- beta-D-glucosaminidase, and (c) the low molecular weight proteinuria p attern. In addition, the histological analysis at the ultrastructural level showed normal glomeruli appearance. The above data suggest that the increased urinary excretion of enzymes and proteins in rats with a cute renal failure is a consequence of tubular injury. Urinary and ser um ACE activities increased and kidney ACE activity decreased. Our dat a suggest that the increase in urine ACE activity may be due to the ki dney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of injury to the proximal t ubule.