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维生素 D 与慢性肾脏病中的血管钙化。

Vitamin D and vascular calcification in chronic kidney disease.

机构信息

Unidad de Investigación, Servicio de Nefrología, Red in ren, Instituto Maimónides de Investigación Biomédica de Córdoba, Departamento de Medicina, Hospital Universitario Reina Sofia, Córdoba, España.

出版信息

Kidney Blood Press Res. 2011;34(4):261-8. doi: 10.1159/000326903. Epub 2011 Jun 21.

Abstract

Vascular calcification is common in patients with chronic kidney disease (CKD) and contributes to the increased rate of cardiovascular morbidity and mortality. The mechanisms regulating vascular calcification are under investigation; it is accepted that vascular calcification is an active and complex process involving many factors that promote or inhibit calcification. Vascular smooth muscle cells undergo transformation into osteogenic cells. This transformation is being stimulated by high phosphate, and more recently the role of the calcium phosphate nanocrystals has gained attention. Experimental models of uremia and in vitro studies have shown that an excess of calcitriol accelerates vascular calcification. However, observational studies suggest that vitamin D provides a survival advantage for patients with CKD. Experimental work shows that for similar serum concentrations of calcium and phosphate paricalcitol produces less vascular calcification than calcitriol suggesting a differential effect at the cellular level. Important issues regarding the role of vitamin D compounds on vascular calcification will be commented in this review.

摘要

血管钙化在慢性肾脏病(CKD)患者中很常见,并且是心血管发病率和死亡率增加的原因。调节血管钙化的机制正在研究中;人们普遍认为血管钙化是一种涉及许多促进或抑制钙化因素的主动且复杂的过程。血管平滑肌细胞向成骨细胞转化。这种转化受到高磷的刺激,最近钙磷纳米晶体的作用也受到了关注。尿毒症的实验模型和体外研究表明,过量的 1,25-二羟维生素 D3(calcitriol)加速了血管钙化。然而,观察性研究表明,维生素 D 为 CKD 患者提供了生存优势。实验工作表明,对于相似的血清钙和磷浓度,帕立骨化醇比 1,25-二羟维生素 D3 产生更少的血管钙化,这表明在细胞水平上存在差异效应。关于维生素 D 化合物对血管钙化作用的重要问题将在本综述中进行讨论。

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