This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

JAMA. 1979;242(17):1875-1876.

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

IT HAS long been known that patients with advanced renal failure require large doses of vitamin D for the expression of its biological effects.¹ The discovery by Fraser and Kodicek² that the kidney is responsible for the production of the active metabolite of vitamin D, 1,25(OH)₂D₃, provided an explanation for the vitamin D-resistant state in patients with chronic uremia and implied that such patients have a deficiency of 1,25(OH)₂D₃. Indeed, Brumbaugh et al³ found that the blood levels of this metabolite in patients with chronic renal failure are low or undetectable.

The successful chemical synthesis of calcitriol made this metabolite available for replacement therapy, and its clinical use has recently been approved for the treatment of patients receiving dialysis.

Since a deficiency of 1,25(OH)₂D₃ is present in patients who have advanced renal failure but who as yet do . . . [Full Text PDF of this Article]

Footnotes
From the Division of Nephrology, Department of Medicine, University of Southern California School of Medicine, Los Angeles.

Reprint requests to Division of Nephrology, University of Southern California School of Medicine, 2025 Zonal Ave, Los Angeles, CA 90033 (Dr Massry).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?