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作 者:廖晟淳 叶朝阳 LIAO Sheng-chun;YE Chao-yang(Department of Nephrology,Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine,Institute of Traditional Chinese Medicine Kidney Disease,Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China)
机构地区:[1]上海中医药大学附属曙光医院肾病科、上海中医药大学中医肾病研究所,上海201203
出 处:《中国血液净化》2023年第8期608-611,共4页Chinese Journal of Blood Purification
基 金:国家自然科学基金面上项目(82170747);华东片区及市级中医专科专病联盟建设项目-肾水病中医专病联盟建设[ZY(2021-2023)-0302]。
摘 要:慢性肾脏病(chronic kidney disease,CKD)-矿物质和骨异常(mineral and bone disorder,MBD)引发的血管钙化(vascular calcification,VC)导致了CKD患者的高心血管死亡率,是CKD重要的临床并发症。骨标志物可观测或参与到VC的过程,对VC的防治起到重要作用。本文将对VC的发生机制进行深入学习,并对常见的骨标志物如甲状旁腺激素(PTH)-25羟维生素D(25-VitD)-成纤维细胞生长因子23(FGF23)-Klotho间的相互反馈影响、骨钙素(osteocalcin,OCN)、I型胶原羧基端肽β特殊序列(carboxy-terminal peptideβspecial sequence,β-CTX)、总Ⅰ型胶原氨基端延长肽(total type I collagen amino-terminal extension peptide,tP1NP)及研究进展做一综述。Vascular calcification(VC)caused by chronic kidney disease-mineral and bone disorder(CKD-MBD)is an important clinical complication,and contributes to the higher cardiovascular mortality in CKD patients.Bone markers can be detected or even involved in the process of VC.Bone markers play important roles in the study of VC.In this paper,we provide an in-depth study of the mechanism of VC,and review the mutual feedback effects among common bone markers such as parathyroid hormone,25-hydroxyvitamin D,fibroblast growth factor 23 and Klotho(PTH-25OHVitD-FGF23-Klotho).We also summarize the recent research progresses in osteocalcin(OCN),type I collagen carboxy-terminal peptideβspecial sequence(β-CTX),and total type I collagen amino-terminal extension peptide(tP1NP).
关 键 词:血管钙化 甲状旁腺激素 25羟维生素D FGF23-Klotho 骨钙素 I型胶原羧基端肽β特殊序列 总Ⅰ型胶原氨基端延长肽
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