Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3-5 has been shown to be as high as 79%. [1] Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease. [1] [2] [3] [4] Alterations in mineral and bone metabolism play a pivotal role in the pathogenesis of vascular calcification in CKD. As CKD progresses, levels of fibroblast growth factor-23 (FGF-23), parathyroid hormone (PTH) and serum phosphorus increase and 1,25-(OH)₂ vitamin D decreases. These imbalances have been linked to the development of vascular calcification. More recently, additional factors have been found to play a role in vascular calcification. Matrix G1a protein (MGP), in the carboxylated form (cMGP), is a potent inhibitor of vascular calcification. Importantly, the carboxylation of MGP is dependent on the co-factor vitamin K. In patients with CKD, vitamin K deficiency is prevalent and is exacerbated by warfarin that is frequently used for anticoagulation. Insufficient bioavailability of vitamin K reduces the amount of cMGP available and therefore may lead to increased risk of vascular calcification. In vitro studies have shown that in the setting of a high phosphorus environment and vitamin K antagonism, human aortic valve interstitial cells become calcified. In this perspective article, we discuss the pathophysiological consequence of vitamin K deficiency in the setting of altered mineral and bone metabolism, its prevalence, and clinical implications in CKD patients.

中文翻译：

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维生素K缺乏症：血管钙化发病机制中的新兴参与者，以及晚期肾脏疾病治疗的医源性后果。

血管钙化是慢性肾脏病（CKD）的已知并发症。非透析依赖性CKD 3-5期患者的血管钙化患病率高达79％。[1]血管钙化与死亡，住院和心血管疾病的风险增加有关。[1] [2] [3] [4]矿物质和骨骼代谢的改变在CKD血管钙化的发病机理中起着关键作用。随着CKD的进展，成纤维细胞生长因子23（FGF-23），甲状旁腺激素（PTH）和血清磷水平升高，而1,25-（OH）₂维生素D减少。这些失衡与血管钙化的发展有关。最近，发现其他因素在血管钙化中起作用。羧基化形式（cMGP）的基质G1a蛋白（MGP）是血管钙化的有效抑制剂。重要的是，MGP的羧化依赖于辅因子维生素K。在CKD患者中，维生素K缺乏症很普遍，并且经常被用于抗凝的华法林加剧了维生素K缺乏症。维生素K的生物利用度不足会降低可用cMGP的量，因此可能导致血管钙化的风险增加。体外研究表明，在高磷环境和维生素K拮抗作用下，人主动脉瓣间质细胞会钙化。在这篇观点文章中，