Studies showing diminished cortical perfusion and reduced glomerular filtration in acute renal failure are apparently at odds with reports of a persistent nephrogram during urography in this disease. We followed the progression of nephrograms in eight dehydrated normal rats, in seven dehydrated rats treated with 12 mg/kg of mercuric chloride (nephrotoxic acute renal failure), and in nine dehydrated rats receiving 5g/kg of IM-glycerol (myoglobinuric acute renal failure). To assess the capacity of our technique to identify a persistent, dense nephrogram, hemorrhagic hypotension (mean arterial pressure, 55–70 mm Hg) was induced in three rats. All rats showed nephrograms on magnification radiographs 1 minute following the injection of 1 cc/lb of sodium diatrizoate. Duplicate coded readings showed no prolongation of nephrograms in ARF-affected animals. Only the hypotensive rats manifested nephrograms on 2-hour radiographs. Some differing characteristics of nephrograms among the groups are explainable on the basis of differences in renal blood flow, as determined in separate experiments. Our findings would favor a preglomerular mechanism as the cause of oliguria in acute renal failure.
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