Rats depleted of renin by chronic saline loading are largely protected from glycerol induced acute renal failure. For some 4 h after glycerol injection, these animals showed the same apparent renal ischemia, cessation of filtration and tubule collapse seen in rats that are not renin depleted. Despite this ischemia, renal function returned rapidly, individual nephron GFR reaching 75 % of normal within the succeeding 12 h. Significant outflow obstruction was evident transiently early in recovery, but was found not to be the prime cause of the low GFR. Recovery of glomerular filtration occurred quickly despite the presence of grossly elevated hydrostatic pressure in some nephrons. It is suggested that renin depletion produced by long term saline ingestion may prevent the protracted afferent arteriolar constriction which is chiefly responsible for the pathophysiologic events in this model of acute renal failure in the rat.

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Hemoglobinuric acute renal failure occurs consistently in rats deprived of water for 24 h and injected with 50% glycerol solution (10 ml/kg) intramuscularly. Severe azotemia developed in 33% of non-dehydrated rats receiving glycerol but 44% were not azotemic, thus permitting a study of the factors which predispose to the development of acute renal failure. There was no necessary correlation between urine volume, urine osmolality, or plasma volume before injection and the development of oliguric acute renal failure, nor was the urine pH during hemoglobinuria correlated with the subsequent severity of azotemia. Plasma volume depletion was the only major difference detected between dehydrated rats which universally developed severe acute renal failure and non-dehydrated rats which were frequently spared. Small differences in plasma volume did not appear to alter the severity of renal involvement in non-dehydrated rats, however.

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