Calcifediol in Chronic Renal Insufficiency
- Jack W. Coburn, MD
- Anthony W. Norman, PhD
Since this article does not have an abstract, we have provided the first 150 words of the full text.
Excerpt
To the Editor.— The reader who is not highly familiar with the recent developments concerning vitamin D and its various active forms may be misled by certain comments made (235: 164, 1976) by Teitelbaum and associates.
First, the major reason for the interest in the treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol (1,25-dihydroxy-vitamin D3 [1,25 {OH}2D3]) and 1α-hydroxycholecalciferol (1α-hydroxy-vitamin D3 [1α {OH} D3]) arises not because of "antirachitic properties of vitamin D in uremia," but because of discoveries that these compounds bypass the necessity for 1-hydroxylation in the kidney.1,2 Thus, the kidney is the only known organ capable of converting 25(OH)D3 to 1,25(OH)2D3, the most active, naturally occurring form of vitamin D; also, 1,25(OH)2D3 may account for all biologic actions heretofore ascribed to vitamin D itself. Moreover, a characteristic of renal osteodystrophy is a resistance to treatment
