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矿物质骨骼异常和血管钙化。

Mineral Bone Abnormalities and Vascular Calcifications.

机构信息

Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO.

Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO; Renal Section, Medicine Service, Rocky Mountain Regional VA Medical Center, Aurora, CO.

出版信息

Adv Chronic Kidney Dis. 2019 Nov;26(6):409-416. doi: 10.1053/j.ackd.2019.09.004.

Abstract

Vascular calcification (VC) is common in chronic kidney disease, increases in prevalence as patients progress to end-stage renal disease, and is significantly associated with mortality. VC is a complex and highly regulated process similar to bone formation whereby hydroxyapatite crystals deposit in the intimal or medial layer of arteries. Mineral bone abnormalities are common in chronic kidney disease; reduction in glomerular filtration rate and changes in vitamin D, parathyroid hormone, and fibroblast growth factor 23 result in the dysregulation of phosphorus and calcium metabolism. Cell culture studies, animal models, and observational and clinical studies all suggest this abnormal mineral metabolism plays a role in the initiation and progression of VC in kidney disease. This review will focus on these mineral bone abnormalities and how they may contribute to mechanisms that induce VC in kidney disease.

摘要

血管钙化(VC)在慢性肾脏病中很常见,随着患者进展为终末期肾病,其患病率增加,并且与死亡率显著相关。VC 是一个复杂且受到高度调节的过程,类似于骨形成,其中羟基磷灰石晶体沉积在动脉的内膜或中膜层。慢性肾脏病中常见矿物质骨骼异常;肾小球滤过率降低和维生素 D、甲状旁腺激素和成纤维细胞生长因子 23 的变化导致磷和钙代谢失调。细胞培养研究、动物模型以及观察性和临床研究均表明,这种异常的矿物质代谢在肾脏病中 VC 的发生和进展中起作用。本综述将重点介绍这些矿物质骨骼异常以及它们如何可能有助于诱导肾脏病中 VC 的机制。

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