The metabolic fate of vitamin D3-3H in chronic renal failure.
The absorption and metabolism of vitamin D(3)-(3)H was studied in eight patients with chronic renal failure. Although the intestinal absorption of vitamin D(3)-(3)H 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 D(3)-(3)H and biologically inactive metabolites. Neither alterations in water-soluble vitamin D(3) metabolites nor qualitative abnormalities in protein-binding of vitamin D(3) were observed in the uremic subjects. Although hemodialysis proved ineffectual in reversing the observed abnormalities in vitamin D(3) 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.
D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001681:Biological Assay; D001806:Blood Urea Nitrogen; D002725:Chloroform; D002762:Cholecalciferol / Q000032:analysis / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002845:Chromatography; D004586:Electrophoresis; D005243:Feces / Q000032:analysis; D005260:Female; D005921:Glomerulonephritis / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000378:metabolism*; D016030:Kidney Transplantation; D008297:Male; D009404:Nephrotic Syndrome / Q000378:metabolism; D011507:Proteinuria; D011704:Pyelonephritis / Q000378:metabolism; D051381:Rats; D006435:Renal Dialysis; D014184:Transplantation, Homologous; D014316:Tritium
D014316:Tritium; D002762:Cholecalciferol; D002725:Chloroform; D000469:Alkaline Phosphatase