Hemodialysis patients with a unique mineralizing defect unresponsive to 1,25-dihydroxycholecalciferol. Dialysis osteomalacic syndrome
Contributions to nephrology, 18, 162-171
Abstract
5 patients are described who developed severe osteomalacia with spontaneous fractures after 2-4 years on dialysis. Phosphate control, vitamin D2 therapy and parathyroidectomy were ineffective. These individuals showed a hypercalcemic tendency but little histologic or radiographic evidence of osteitis fibrosa. After parathyroidectomy, the hypercalcemic tendency remained and bone biopsy revealed gross osteomalacia. A 6- to 12-month therapeutic trial with 1,25-dihydroxycholecalciferol (1,25[OH]2D3) in 3 did not arrest skeletal deterioration. 4 subsequently developed dialysis encephalopathy. These patients appear to have a unique mineralizing defect unresponsive to 1,25(OH)2D3. This "dialysis osteomalacic syndrome" may result from toxic substances associated with uremia or the hemodialysis regimen.
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Cite this article
E C Cameron, J C Prior, & H S Ballon (1900). Hemodialysis patients with a unique mineralizing defect unresponsive to 1,25-dihydroxycholecalciferol. Dialysis osteomalacic syndrome. *Contributions to nephrology*, *18*, 162-171. https://doi.org/10.1159/000403284
E C Cameron, J C Prior, H S Ballon. Hemodialysis patients with a unique mineralizing defect unresponsive to 1,25-dihydroxycholecalciferol. Dialysis osteomalacic syndrome. Contrib Nephrol. 1900;18:162-171. doi:10.1159/000403284
E C Cameron, et al. "Hemodialysis patients with a unique mineralizing defect unresponsive to 1,25-dihydroxycholecalciferol. Dialysis osteomalacic syndrome." *Contributions to nephrology*, vol. 18, 1900, pp. 162-171.
Keywords
Adult, Alkaline Phosphatase, Bone Diseases, Calcium, Clinical Trials As Topic, Dihydroxycholecalciferols, Ergocalciferols, Female, Humans, Hydroxycholecalciferols, Kidney Failure, Chronic, Male, Middle Aged, Parathyroid Glands, Parathyroid Hormone, Renal Dialysis