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The Efficacy of Calcifediol in Renal Osteodystrophy

Robert Recker, MD; Patricia Schoenfeld, MD; Joseph Letteri, MD; Eduardo Slatopolsky, MD; Ralph Goldsmith, MD; Arnold Brickman, MD
Arch Intern Med. 1978;138(Suppl_5):857-863. doi:10.1001/archinte.1978.03630300025005.
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Bone disease continues to be a problem for patients who are undergoing long-term hemodialysis.1-4 Although the clinical syndrome of renal osteodystrophy varies from center to center and from patient to patient, it is generally believed that disturbances in vitamin D metabolism are almost always present and play a pivotal role in its pathogenesis. Most patients demonstrate at least some clinical, biochemical, or histological evidence of vitamin D resistance.1-7

The two principal circulating vitamin D metabolites are 25-hydroxyvitamin D (25OHD) (25OHD refers to 25OHD2 and 25OHD3 since the assay does not differentiate between either of these), the liver product, and 1,25-dihydroxyvitamin D (1,25[OH]2D), the kidney product.7 Most investigators have focused attention on the latter since it is the final step in vitamin D synthesis, it is the most potent form of vitamin D, and it is synthesized by the kidney.7 Indeed, 1,25(OH)2


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