Cournot-Witmer G, Zingraff J, Plachot J J, Escaig F, Lefèvre R, Boumati P, Bourdeau A, Garabédian M, Galle P, Bourdon R, Drüeke T, Balsan S
Kidney Int. 1981 Sep;20(3):375-8. doi: 10.1038/ki.1981.149.
It has been suggested that in uremic bone, aluminum interferes with normal mineralization. Aluminum content and aluminum localization were studied in iliac crest biopsies of two groups of patients on regular hemodialysis; one group had histologic osteomalacia, and little or no bone resorption (group 1); the other, osteitis fibrosa and no mineralization defect (group 2). Group 1 patients had significantly higher plasma aluminum concentrations than those of group 2. No difference was found in bone aluminum content, which was above normal in both groups. In the bone samples of the osteomalacic subjects, aluminum was mainly localized at the limit between osteoid and calcified tissue, the site where the bone mineral is normally first deposited. Osteomalacia could not be related to hypocalcemia or to phosphate depletion. Active vitamin D derivatives (25-hydroxycholecalciferol and 1alpha-hydroxycholecalciferol) failed to prevent or to improve the bone disease. In the bone samples of group 2 subjects, aluminum could not be localized by the methods used, except in the two cases with greatly elevated bone aluminum, where it was mainly localized on cement lines. In group 2 subjects, immunoreactive parathyroid hormone plasma concentration, osteoclast surface, and marrow fibrosis were significantly higher than they were in group 1 subjects. It is concluded that in bone from uremic patients on regular dialysis, aluminum can induce a particular form of osteomalacia, resistant to the vitamin D active derivatives. The bone disease is only observed in the absence of severe secondary hyperparathyroidism. This suggests that parathyroid hormone may be involved in the development of the aluminum-induced mineralization defect.
有人提出，在尿毒症骨中，铝会干扰正常矿化。对两组定期进行血液透析的患者的髂嵴活检组织进行了铝含量和铝定位研究；一组有组织学上的骨软化症，几乎没有或没有骨吸收（第1组）；另一组有纤维性骨炎且无矿化缺陷（第2组）。第1组患者的血浆铝浓度明显高于第2组。两组的骨铝含量均高于正常水平，未发现差异。在骨软化症患者的骨样本中，铝主要定位于类骨质和钙化组织之间的界限处，即正常情况下骨矿物质首先沉积的部位。骨软化症与低钙血症或磷酸盐缺乏无关。活性维生素D衍生物（25-羟胆钙化醇和1α-羟胆钙化醇）未能预防或改善骨病。在第2组患者的骨样本中，除了两例骨铝含量大幅升高的病例外，所用方法未能定位铝，在这两例中铝主要定位于黏合线。第2组患者的免疫反应性甲状旁腺激素血浆浓度、破骨细胞表面和骨髓纤维化明显高于第1组患者。得出的结论是，在定期透析的尿毒症患者的骨骼中，铝可诱发一种对维生素D活性衍生物有抗性的特殊形式的骨软化症。这种骨病仅在无严重继发性甲状旁腺功能亢进的情况下观察到。这表明甲状旁腺激素可能参与了铝诱导的矿化缺陷的发生发展。
