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[慢性肾脏病患者发生心血管事件时磷和钙稳态紊乱的机制。成纤维细胞生长因子23和klotho的作用]

[Mechanisms of phosphorus and calcium homeostatic disorders in the development of cardiovascular events in patients with chronic renal diseases. The role of fibroblast growth factor 23 and Klotho].

作者信息

Milovanova L Iu, Kozlovskaia L V, Milovanov Iu S, Bobkova I N, Dobrosmyslov I A

出版信息

Ter Arkh. 2010;82(6):66-72.

Abstract

The paper deals with the analysis of studies of the role of the bone morphogenetic proteins fibroblast growth factor 23 (FGF-23) and Klothno in the development of vascular wall calcification in chronic renal disease (CRD). FGF-23 is shown to be an important phosphaturic hormone that inhibits hypercalcemic and hyperphosphatemic effects of elevated serum vitamin D concentrations. There is evidence that there is an association between high serum FGF-23 levels and vascular wall calcification irrespective of the content of phosphorus and parathyroid hormone. Most authors regard FGF-23 as a potential uremic toxin in patients with end-stage CRD. There are data that support the renoprotective value of the morphogenetic protein Klotho whose expression in CRD is decreased.

摘要

本文探讨了骨形态发生蛋白、成纤维细胞生长因子23(FGF - 23)和α-klotho在慢性肾病(CRD)血管壁钙化发展过程中作用的研究分析。FGF - 23被证明是一种重要的磷调节激素,可抑制血清维生素D浓度升高所产生的高钙血症和高磷血症效应。有证据表明,无论磷和甲状旁腺激素的含量如何,血清FGF - 23水平升高与血管壁钙化之间存在关联。大多数作者认为FGF - 23是终末期CRD患者潜在的尿毒症毒素。有数据支持形态发生蛋白α-klotho的肾脏保护价值,其在CRD中的表达降低。

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