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[胶原代谢与尿毒症性骨矿化——肾性骨营养不良的分子病理学研究]

[Collagen metabolism and mineralization of uremic bone--aspects of the molecular pathology of renal osteodystrophy].

作者信息

Heidbreder E, Lüke F, Heidland A

出版信息

Klin Wochenschr. 1976 Apr 15;54(8):341-8. doi: 10.1007/BF01469788.

Abstract

Importance sequelae of uremia are hormonal changes in calcium homeostasis combined with chronic calcium imbalance causing structural alteration and functional insufficiency of bone. Morphological findings of the so called renal osteodystrophy are osteomalacia, osteitis fibrosa and osteoporosis. Osteitis fibrosa and abnormal skeletal metabolism (changes of collagen turnover, insufficient maturation of stable bone crystals) impair the mechanical qualities of bone. Probably the uremia per se influences the collagen metabolism; additional factors such as secondary hyperparathyroidism and deficiency of vitamin D3 are discussed.

摘要

尿毒症的重要后遗症是钙稳态的激素变化,伴有慢性钙失衡,导致骨骼结构改变和功能不全。所谓肾性骨营养不良的形态学表现为骨软化、纤维性骨炎和骨质疏松症。纤维性骨炎和异常的骨骼代谢(胶原周转变化、稳定骨晶体成熟不足)损害了骨骼的机械性能。尿毒症本身可能影响胶原代谢;还讨论了继发性甲状旁腺功能亢进和维生素D3缺乏等其他因素。

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