Azotemic osteodystrophy - indications for intervention.
Because the pathogenetic mechanisms leading to azotemic osteodystrophy are incompletely understood, prophylactic and therapeutic intervention must necessarily be less than satisfactory. There is no proof that prophylactic measures, e.g. phosphate binders and vitamin D (metabolites) are beneficial in incipient renal failure but measures to prevent secondary hyperparathyroidism appear reasonable. In advanced renal failure, oral phosphate binders, administration of calcium salts and vitamin D (metabolites) are effective in returning serum chemistry towards normal, but considerably less effective in restoring normal bone histology. Hemodialysis, using adequate calcium concentrations in the dialysate, permits one to normalize predialytic calcium and phosphorus levels, and maintain calcium balance in the majority of patients. Hemodialysis does not, however, prevent hyperparathyroidism and the various types of metabolic bone disease. Symptomatic azotemic osteodystrophy increases in frequency and severity with increasing duration of dialysis. While osteitis fibrosa responds favorably to vitamin D and several vitamin D metabolites, osteomalacia is considerably less responsive. It remains unknown whether this is due to low bone turnover, absence of some crucial unknown vitamin D metabolite, or involvement of non-vitamin D-related factors. Parathyroidectomy for uncontrollable hyperparathyroidism is required only in a minority of patients.
D001847:Bone Diseases / Q000209:etiology / Q000628:therapy*; D002118:Calcium / Q000097:blood; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications / Q000628:therapy*; D010280:Parathyroid Glands / Q000601:surgery; D010710:Phosphates / Q000097:blood; D006435:Renal Dialysis; D014511:Uremia / Q000150:complications / Q000628:therapy*; D014807:Vitamin D / Q000378:metabolism
D010710:Phosphates; D014807:Vitamin D; D002118:Calcium