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Aspirin-Induced Depression of Glomerular Filtration Rate in Normal Humans: Role of Sodium Balance

RICHARD S. MUTHER, M.D.; DONALD M. POTTER, M.D.; and WILLIAM M. BENNETT, M.D.
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Presented in part 12 May 1980, at the national meeting of the American Federation for Clinical Research.

▸ Requests for reprints should be addressed to William M. Bennett, M.D.; Division of Nephrology, University of Oregon Health Sciences Center; 3181 S.W. Sam Jackson Park Road; Portland, OR 97201.


Portland, Oregon


© 1981 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1981;94(3):317-321. doi:10.7326/0003-4819-94-3-317
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The renal clearance of endogenous creatinine, inulin and para-aminohippurate was measured in 10 healthy human volunteers taking aspirin during severe dietary sodium restriction (10 meq/d) to clarify the clinical significance and pathophysiology of aspirin-induced changes in renal function. Sodium restriction alone had no effect on renal clearances but did increase plasma renin activity and urinary prostaglandin E excretion. The addition of aspirin decreased the urinary clearance of prostaglandin E but not plasma renin activity, and caused a significant fall in both endogenous creatinine (from 92.3 ±4.1 SE mL/ min · 1.73 m2 body surface area to 80.8 ± 4.4 mL/min · 1.73 m2, p=0.02) and inulin (from 95.3 ± 7.0 mL/min · 1.73 m2 to 80.9 ± 7.0 mL/min · 1.73 m2, p < 0.001). The fall in inulin clearance was directly related to the salicylate level. The clearance of para-aminohippurate showed only a slight, statistically insignificant decline with aspirin. The results of this study suggest that aspirin-induced depression of glomerular filtration rate may be independent of total renal plasma flow. Aspirin should be used cautiously, with careful attention to dosage, in sodium-restricted patients whose glomerular filtration rate may, in part, be under the homeostatic control of renal prostaglandins.

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