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Research Article Free access | 10.1172/JCI105909

The metabolic fate of vitamin D3-3H in chronic renal failure

Louis V. Avioli, Stanley Birge, Sook Won Lee, and Eduardo Slatopolsky

1Renal and Endocrine Divisions, Department of Medicine, Washington University School of Medicine, and The Jewish Hospital of St. Louis, St. Louis, Missouri 63110

Find articles by Avioli, L. in: JCI | PubMed | Google Scholar

1Renal and Endocrine Divisions, Department of Medicine, Washington University School of Medicine, and The Jewish Hospital of St. Louis, St. Louis, Missouri 63110

Find articles by Birge, S. in: JCI | PubMed | Google Scholar

1Renal and Endocrine Divisions, Department of Medicine, Washington University School of Medicine, and The Jewish Hospital of St. Louis, St. Louis, Missouri 63110

Find articles by Lee, S. in: JCI | PubMed | Google Scholar

1Renal and Endocrine Divisions, Department of Medicine, Washington University School of Medicine, and The Jewish Hospital of St. Louis, St. Louis, Missouri 63110

Find articles by Slatopolsky, E. in: JCI | PubMed | Google Scholar

Published October 1, 1968 - More info

Published in Volume 47, Issue 10 on October 1, 1968
J Clin Invest. 1968;47(10):2239–2252. https://doi.org/10.1172/JCI105909.
© 1968 The American Society for Clinical Investigation
Published October 1, 1968 - Version history
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Abstract

The absorption and metabolism of vitamin D3-3H was studied in eight patients with chronic renal failure. Although the intestinal absorption of vitamin D3-3H was normal, the metabolic fate of the vitamin was abnormal as characterized by a twofold increase in fractional turnover rate, an abnormal accumulation of biologically inactive lipid-soluble metabolites, and the urinary excretion of both vitamin D3-3H and biologically inactive metabolites. Neither alterations in water-soluble vitamin D3 metabolites nor qualitative abnormalities in protein-binding of vitamin D3 were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D3 metabolism and excretion, renal homotransplantation was completely successful in this regard. These experiments support the conclusion that the resistance to therapeutic doses of vitamin D often seen in patients with chronic renal failure and renal osteodystrophy results from an acquired defect in the metabolism and excretion of vitamin D.

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