Renal excretion of uric acid during prolonged fasting

  • Irving H. Fox
    Correspondence
    Reprint requests should be addressed to Dr. I.H. Fox, University of Toronto Rheumatic Disease Unit, The Wellesley Hospital, 160 Wellesley St. East, Toronto, Ontario, Canada.
    Footnotes
    Affiliations
    Division of Rheumatology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Nephrology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Endocrinology, Department of Medicine, University of Toronto, Ontario, Canada.
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  • Mitchell L. Halperin
    Affiliations
    Division of Rheumatology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Nephrology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Endocrinology, Department of Medicine, University of Toronto, Ontario, Canada.
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  • Marc B. Goldstein
    Affiliations
    Division of Rheumatology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Nephrology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Endocrinology, Department of Medicine, University of Toronto, Ontario, Canada.
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  • Errol B. Marliss
    Affiliations
    Division of Rheumatology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Nephrology, Department of Medicine, University of Toronto, Ontario, Canada.

    Division of Endocrinology, Department of Medicine, University of Toronto, Ontario, Canada.
    Search for articles by this author
  • Author Footnotes
    1 Dr. Fox is a Research Associate of the Canadian Arthritis and Rheumatism Society.
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      Abstract

      Serum and urine uric acid were evaluated during prolonged therapeutic fasting in 15 obese patients. With increasing ketonemia the serum uric acid rose from a control value of Math Eq at 7 days and then decreased progressively to Math Eq by 28 days despite sustained ketonemia. The uric acid clearances were 5.5 ± 0.9, 1.8 ± 0.2, and 4.4 ± 1.5 ml/min at days 0, 7, and 28 of fasting. At the same times the creatinine clearances were 114 ± 11, 80 ± 6, and 64 ± 6.3 ml/min. There was no evidence of a renal tubular abnormality as assessed by glycosuria, bicarbonaturia, or increased phosphaturia. Urate binding to plasma proteins remained unchanged. Acute studies of the renal handling of uric acid revealed a uricosuric response to the administration of sodium lactate or sodium bicarbonate by intravenous infusion and low-dose acetylsalicylic acid orally. This renal tubular response departs significantly from that observed during the overnight fasted state and could not be accounted for by extracellular fluid volume expansion or the induced acid-base changes.
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