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A method is presented for the production of a reproducible and reversible renal lesion in the rat by the intravenous injection of a relatively small amount of homologous hemoglobin (40 mg/100 g body weight). Production of the lesion is dependent on prior water deprivation and its severity is related to the degree of dehydration. Ether anesthesia, at the time of hemoglobin injection, predisposes to a severe and reproducible functional defect in the dehydrated rat. In contrast, injection of hemoglobin during pentobarbital anesthesia results in a significant lesion only sporadically. The functional evolution of the lesion has been characterized by inulin clearance measurements. Functional impairment occurs abruptly, within 1 hr after hemoglobin injection, and persists unchanged over the ensuing several hours. Some increase in inulin clearance rate is usually observed at 24 hr after injection, but severe functional impairment persists. Between 24 and 72 hr, a considerable increase in inulin clearance rate occurs, so that only moderate restriction of excretory function is present at the latter time. A further moderate increase in inulin clearance rate is apparent at 7 days after hemoglobin injection, but some reduction in function. persisted in all rats studied at this time. Hemoglobinuria is slight or inapparent in animals manifesting the most marked depression of excretory function, indicating that a severe renal lesion may exist in the absence of visible urinary pigment. Hemoglobinemia is evanescent at the dosage used in this study. These observations suggest that clinical acute renal failure secondary to hemoglobinemia may readily go unrecognized and that this may be a more frequent association than is now appreciated.
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