AJP - Renal Physiology, Vol 261, Issue 1 14-F21, Copyright © 1991 by American Physiological Society

ARTICLES

Impaired renal hemodynamic response to protein feeding in dogs with experimental Fanconi syndrome

L. L. Woods and E. W. Young
Division of Nephrology and Hypertension, Oregon Health Sciences University, Portland 97201.

These studies were designed to test the hypothesis that intact proximal tubular function is required for protein-stimulated renal vasodilation. In normal chronically instrumented conscious dogs, a meal of raw beef (10 g/kg) caused glomerular filtration rate (GFR) to increase significantly from 63 +/- 5 to 94 +/- 10 ml/min after 90 min, while plasma alpha-amino nitrogen rose from 3.9 +/- 0.2 to 6.7 +/- 0.6 mg/dl. In another group of dogs experimental Fanconi syndrome (generalized proximal tubular dysfunction) was induced with maleic acid (25 mg/kg iv, pH 7.3). GFR fell slightly but significantly from 91 +/- 18 to 66 +/- 9 ml/min after maleic acid, while Na+ excretion rose from 24 +/- 8 to 176 +/- 24 mu eq/min, alpha-amino nitrogen excretion rose from 82 +/- 40 to 148 +/- 47 micrograms/min, and glucose excretion rose from 0.2 +/- 0.1 to 6.1 +/- 1.0 mg/min. In response to a subsequent meat meal, plasma alpha-amino nitrogen rose significantly from 3.8 +/- 0.4 to 6.2 +/- 0.5 mg/dl, but GFR did not change, averaging 66 +/- 9 ml/min over the next 120 min. These results suggest that normal proximal tubular function is necessary for protein-stimulated renal vasodilation to occur. This finding is consistent with the hypothesis that the tubuloglomerular feedback mechanism may be involved in mediating the normal renal hemodynamic response to protein feeding.

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