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July 26, 1976

Calcifediol in Chronic Renal Insufficiency

Author Affiliations

Veterans Administration Wadsworth Hospital Center UCLA School of Medicine Los Angeles
University of California at Riverside Riverside

JAMA. 1976;236(4):347. doi:10.1001/jama.1976.03270040013015

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