Co-Authors:
Lubetsky, A., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Winaver, J., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Seligmann, H., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Olchovsky, D., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Almog, S., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Halkin, H., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel
Ezra, D., Department of Medicine, Division of Clinical Pharmacology, Sheba Medical Center, Tel-Hashomer, Israel, Tel Aviv Univ. School of Medicine, Department of Renal Physiology, Technion School of Medicine, Haifa, Israel, Department of Medicine A, Sheba Medical Center, Tel-Hashomer 52621, Israel
Abstract:
Long-term furosemide therapy is associated with increased urinary loss of thiamine. To examine the mechanism of furosemide-induced urinary thiamine loss, we measured urinary excretion of thiamine in rats in response to increasing doses of furosemide, acetazolamide, chlorothiazide, amiloride, mannitol, and extracellular fluid (ECF) volume loading by saline infusion. All animals were in normal thiamine balance as reflected by a thiamine pyrophosphate effect (TPPE) of 2.25% ± 0.60% (mean ± SEM), and all had normal renal function. Urinary flow increased in response to diuretic administration in a dose-dependent manner, reaching (mean) peak urinary flow rates of 283 to 402 μL/min. Fractional excretion of sodium (FE(Na)) exhibited the same pattern, reaching peak values of 12.3% to 23.2%. Urinary thiamine excretion increased in proportion to the incremental doses of diuretic agents, reaching (mean) maximal values of 7.44 to 9.34 pmol/min, with no significant difference (P = .11) between the various diuretics tested nor in response to saline loading. None of the diuretics tested differed in the effect on thiamine excretion, which was clearly flow dependent and only partially related to fractional sodium excretion. Urinary flow rate, being the single significant predictor, explained 78% (R2 = 0.78) of the variability in thiamine excretion rates. These findings indicate that urinary thiamine loss is caused by a nonspecific, flow-dependent mechanism common to all of the diuretics tested.
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