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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.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
From the Departments of Medicine, Creighton University, Omaha (Dr Recker), University of California, San Francisco (Drs Schoenfeld and Brickman), State University of New York at Stoney Brook (Dr Letteri), Washington University, St Louis (Dr Slatopolsky), and University of Texas at San Antonio (Dr Goldsmith).

Footnotes
Read before The Upjohn Co, Kalamazoo, Mich, Nov 2, 1976.

Reprint requests to 10th and Castelar, Omaha, NE 68178 (Dr Recker).

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