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

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 6to 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 1,25-dihydroxycholecalciferol unresponsive, Prior JC dialysis osteomalacic syndrome, hemodialysis patients mineralizing defect spontaneous fractures, renal osteodystrophy osteomalacia vitamin D resistant, dialysis encephalopathy osteomalacia association, parathyroidectomy hypercalcemia hemodialysis osteomalacia, Cameron Prior Ballon dialysis bone disease, 1,25-dihydroxyvitamin D3 resistant osteomalacia dialysis, uremic toxin bone mineralization defect hemodialysis, severe osteomalacia hemodialysis aluminum toxicity
PMID 6986229 6986229 DOI 10.1159/000403284 10.1159/000403284

Cite this article

E C Cameron, J C Prior, & H S Ballon (1980). 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