Cushner H M, Adams N D
Am J Med Sci. 1986 Apr;291(4):264-75. doi: 10.1097/00000441-198604000-00008.
Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
纤维性骨炎和骨软化症的组织学骨改变在终末期肾病患者中很常见。尽管许多患者没有因这些骨改变而出现症状，但一些患者会严重致残。肾衰竭时维生素D、钙、磷和甲状旁腺激素的代谢发生改变，这有助于尿毒症骨病的发展。本文综述了目前关于肾性骨营养不良发病机制和治疗的理论。此外，还讨论了尿毒症中各种铝相关性骨软化综合征的临床表现、发病机制和治疗。
