慢性肾脏病-矿物质和骨代谢紊乱导致血管钙化的分子机制研究进展

慢性肾脏病-矿物质和骨代谢紊乱(CKD-MBD)所导致的血管钙化是增加CKD患者发生心血管事件的独立危险因素。钙磷平衡的破坏、氧化应激的增加、钙化抑制剂的丢失、RANKL表达的增加等均被认为与CKD患者血管钙化的发生有关。此外,受损的骨质能够进一步扰乱血清钙磷和甲状旁腺激素水平,从而促进CKD患者发生血管钙化。磷结合剂和双膦酸盐类药物是目前治疗CKD-MBD所致的血管钙化是治疗的常用方法,可以改善骨质疏松以及血管钙化。本文就近年来CKD-MBD血管钙化发生机制的研究进展进行了综述。

Research Progress of Molecular Mechanisms of Vascular Calcification in CKD-MBD

ABSTRACT: Chronic kidney disease-mineral and bone disorder (CKD-MBD)-induced vascular calcification has been proved to be an independent risk factor of cardiovascular events in patients with chronic kidney disease (CKD). Impaired calcium and phosphate homeostasis, increased oxidative stress, loss of calcification inhibitors and increased expression of RANKL are related to the vascular cal- cification in CKD. Additionally, impaired bone may be implicated in the pathogenesis of vascular calcification through perturbing serum calcium/phosphate and parathyroid hormone, thus contributing to increased vascular calcification in CKD. Therapeutic approaches for CKD, such as phosphate binders and bisphosphonates, have been shown to ameliorate bone loss as well as vascular calcification. This ar- ticle reviews recent progress of the pathogenesis of vascular calcification in CKD-MBD.