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The role of the concentrating mechanism in the potentiation of acute renal failure by dehydration has been studied using rats with complete diabetes insipidus. These rats were shown to be continually dehydrated even when allowed free access to water. Despite massive volumes of highly dilute urine at the time that hemoglobinuria was induced by glycerol injection, these animals developed acute renal insufficiency whose severity was intermediate between that of non-dehydrated and severely dehydrated normal rats treated similarly. Micropuncture experiments showed the appearance of the kidney in vivo and the functional abnormalities of the three types of rats to be qualitatively identical. It appears that dehydration’s effect on hemoglobinuric acute renal failure is independent of the concentrating mechanism and correlates well with plasma volume depletion. It is suggested that factors other than ADH titre, high urine concentration and low flow rate are the prime determinants of the effect of dehydration on hemoglobinuric acute renal failure in the rat.

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-de