Vitamin D and the syndromes of azotaemic osteodystrophy.
Intestinal malabsorption of calcium and the development of osteomalacia in conservatively treated renal failure is explained by a quantitative deficiency of 1,25-dihydroxycholecalciferol, which also contributes to the development of hypocalcaemia. Excess of 25-hydroxycholecalciferol can substitute for this deficiency. The presence and healing of azotaemic osteomalacia is unrelated to the prevailing plasma [Ca] x [P] product. The data suggest that "vitamin D" acts directly on bone mineralisation, but the claim that this apparent effect is normally due to 25-hydroxycholecalciferol is considered unproven. Most of the phenomena of azotaemic osteodystrophy are encountered in simple vitamin D deficiency; as in that condition, deficiency of 1,25-dihydroxycholecalciferol may be of primary significance in causing secondary hyperparathyroidism in renal failure.
D001862:Bone Resorption; D002118:Calcium / Q000097:blood; D004100:Dihydroxycholecalciferols / Q000378:metabolism; D004351:Drug Resistance; D004872:Ergocalciferols / Q000627:therapeutic use; D006801:Humans; D007011:Hypoparathyroidism / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000378:metabolism*; D010710:Phosphates / Q000097:blood; D011547:Pseudohypoparathyroidism / Q000503:physiopathology; D014511:Uremia / Q000378:metabolism*; D014807:Vitamin D / Q000378:metabolism*
D004100:Dihydroxycholecalciferols; D004872:Ergocalciferols; D010710:Phosphates; D014807:Vitamin D; D002118:Calcium