Increasing doses of intravenous uranyl nitrate above 2.5 mg/kg of body weight result in more extensive renal tubular necrosis without increasing azotemia in the rat. Despite a uniform level of azotemia, renal tubular epithelial dysfunction tended to parallel the changes in renal tubular pathology. Saline loading, designed to suppress the renin–angiotensin system, ameliorated the azotemia but not the tubular necrosis or tubular dysfunction after uranyl nitrate. These results suggest that passive backflow of glomerular filtrate through necrotic tubular epithelium is not responsible for the azotemia after uranyl nitrate in the rat. The protection afforded by saline loading further suggests a role for the renin–angiotensin system in the development of uranyl nitrate induced acute renal failure.
|Original language||English (US)|
|Number of pages||7|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - May 1973|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)