Cameron E C, Prior J C, Ballon H S
Contrib Nephrol. 1980;18:162-71. doi: 10.1159/000403284.
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.
本文描述了5例患者,他们在透析2至4年后出现了严重的骨软化症并伴有自发性骨折。磷酸盐控制、维生素D2治疗和甲状旁腺切除术均无效。这些患者表现出高钙血症倾向,但很少有纤维性骨炎的组织学或影像学证据。甲状旁腺切除术后,高钙血症倾向依然存在,骨活检显示有明显的骨软化症。对其中3例患者进行了为期6至12个月的1,25 - 二羟胆钙化醇(1,25[OH]2D3)治疗试验,但并未阻止骨骼恶化。4例患者随后出现了透析性脑病。这些患者似乎有一种独特的矿化缺陷,对1,25(OH)2D3无反应。这种“透析性骨软化综合征”可能是由与尿毒症或血液透析方案相关的有毒物质引起的。