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Diminished Renal Urate Secretion Per Nephron As a Basis for Primary Gout

RICHARD E. RIESELBACH, M.D., F.A.C.P.; LEIF B. SORENSEN, M.D.; WELDON D. SHELP, M.D.; and THOMAS H. STEELE, M.D.
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Presented at the IVth International Congress of Nephrology, June 1969, Stockholm, Sweden, and published in abstract form in J Clin Invest 47:1108, 1967

▸Requests for reprints should be addressed to Richard E. Rieselbach, M.D., Department of Medicine, University Hospitals, 1300 University Avenue, Madison, Wis. 53706


Madison, Wisconsin; and Chicago, Illinois


Ann Intern Med. 1970;73(3):359-366. doi:10.7326/0003-4819-73-3-359
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In order to examine the role of the kidney in the pathogenesis of primary gout, the rate of uric acid turnover and renal transport were studied in 15 gouty patients. Uric acid turnover data from nine control subjects were the basis for classifying gouty patients as either overproducers or normoproducers. The pyrazinamide suppression test provided comparison of renal rates of urate reabsorption and secretion between the two groups in the presence of both endogenous hyperuricemia and allopurinol-induced normouricemia. Both groups had a normal pattern of urate reabsorption over a wide range of filtered loads. However, whereas the pattern of urate secretion in gouty overproducers could not be distinguished from previously published data in normals, diminished urate secretion was evident in normoproducers during hyperuricemia. This insufficient secretory response may limit the capacity for urate homeostasis and thereby provide the basis for hyperuricemia in some patients with primary gout without demonstrable overproduction of uric acid.

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