A scanning electron microscopic study of the glycerol model of acute renal failure.

Previous studies have implicated both intrarenal vasconstriction and reduced glomerular permeability in the pathogenesis of acute renal failure. Studies were performed to examine further the role of vasconstriction and glomerular structural abnormalities in this syndrome. Six rats (group I) given angiotensin II (180 ng. per 100 gm. per minute) did not develop acute renal failure (blood urea nitrogen 28.6 mg. per 100 ml. at 24 hours). Twenty-five rats (group II), allowed free access to water and given glycerol intramuscularly (8 ml. per kg.), developed mild acute renal failure (blood urea nitrogen 41.6 mg. per 100 ml. at 24 hours). Ten nondehydrated rats (group III), given both glycerol and angiotensin II, developed a more severe form of acute renal failure (blood urea nitrogen 120.4 mg. per 100 ml. at 24 hours p less than 0.001); this value was not significantly different from that of 14 rats (group IV) dehydrated 24 hours prior to glycerol administration (blood urea nitrogen 137 mg. per 100 ml. at 24 hours).