Acute renal failure was produced in vasopressin-pretreated rabbits by clamping the left renal pedicle for 1 hr and removing the opposite kidney. Treatment with clonidine, an antihypertensive drug that blunts the kidney's response to vasopressin, resulted in significantly higher creatinine clearance and urine flow rate in the first 6 hr after unclamping. Clonidine (30 μg/kg given intravenously 30 min before unclamping) also significantly lessened the number of hyaline casts in outer medullary tubules and inner medullary loops of Henle 6 hr after unclamping and reduced the number of abnormal tubular contours in microradiograms produced by infusing barium sulfate into the renal artery at sufficient pressure to rupture glomerular capillaries, causing an escape of contrast material into the tubules. The spaces consistently observed between the ends of barium columns and hyaline casts in microdissection studies and the great lengths of the hyaline casts suggest that hyaline casts obstruct the flow of tubular fluid. Clonidine treatment resulted in fewer, shorter, and thinner hyaline casts. These results indicate that tubular obstruction by hyaline casts plays an important role in early postischemic acute renal failure, and that clonidine's beneficial effect is due in part to a reduction in cast formation.
|Original language||English (US)|
|Number of pages||28|
|Journal||American Journal of Pathology|
|State||Published - Jan 1 1980|
ASJC Scopus subject areas
- Pathology and Forensic Medicine