Hemodialysis patients with a unique mineralizing defect unresponsive to 1,25-dihydroxycholecalciferol. Dialysis osteomalacic syndrome

Contributions to nephrology, 18, 162-171

DOI 10.1159/000403284 PMID 6986229 Source

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.

Topics

dialysis osteomalacia syndrome, hemodialysis bone disease vitamin d, renal failure mineralizing defect, dialysis encephalopathy bone disease, calcitriol resistant osteomalacia, uremic bone disease parathyroidectomy, chronic kidney disease mineral disorder

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

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