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[血管钙化——病理机制与临床应用——. 慢性肾脏病 - 矿物质和骨异常(CKD-MBD)中的血管钙化]

[Vascular Calcification - Pathological Mechanism and Clinical Application - . Vascular calcification in chronic kidney disease-mineral and bone disorder (CKD-MBD)].

作者信息

Omata Momoyo, Fukagawa Masafumi, Kakuta Takatoshi

机构信息

Department of Internal Medicine, Hachioji Azumacho Clinic, Tokyo, Japan.

出版信息

Clin Calcium. 2015 May;25(5):645-53.

PMID:25926567
Abstract

Chronic kidney disease-mineral and bone disorder (CKD-MBD), is sequential pathophysiology that starts in the very early stages of CKD. Three major aspects of CKD-MBD are laboratory abnormalities, bone abnormalities and vascular calcification. In dialysis patients, the prevalence of death due to cardiovascular disease accounts for more than 40% of all-cause mortality. Therefore, arteriosclerosis with vascular calcification may be an important pathophysiological mechanism in the development of cardiovascular disease. Vascular calcification is known to be an important risk factor influencing mortality in CKD patients. A number of studies have suggested a close association between serum FGF23 concentration and the risks of mortality, cardiovascular disease vascular calcification as well as CKD progression. Renal insufficiency leads to decline in klotho level and impaired phosphate excretion. However serum phosphate levels are maintained in the normal range by up regulation of FGF23 and PTH in early CKD stage. Early treatment intervention is necessary to improve the prognosis of the CKD patient.

摘要

慢性肾脏病 - 矿物质和骨异常(CKD - MBD)是一种在CKD早期阶段就开始的连续病理生理学过程。CKD - MBD的三个主要方面是实验室检查异常、骨异常和血管钙化。在透析患者中,心血管疾病导致的死亡患病率占全因死亡率的40%以上。因此,伴有血管钙化的动脉硬化可能是心血管疾病发生发展的重要病理生理机制。血管钙化是影响CKD患者死亡率的重要危险因素。多项研究表明,血清FGF23浓度与死亡率、心血管疾病、血管钙化以及CKD进展风险密切相关。肾功能不全导致klotho水平下降和磷排泄受损。然而,在CKD早期阶段,通过FGF23和甲状旁腺激素(PTH)的上调,血清磷水平维持在正常范围内。早期治疗干预对于改善CKD患者的预后是必要的。

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