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Vitamin K in CKD Bone Disorders
Calcified Tissue International ( IF 4.2 ) Pub Date : 2021-01-06 , DOI: 10.1007/s00223-020-00792-2
M Fusaro 1, 2 , G Cianciolo 3 , P Evenepoel 4 , L Schurgers 5 , M Plebani 6
Affiliation  

Vitamin K is principally known because it is involved in blood coagulation. Furthermore, epidemiological studies showed that its deficit was associated with increased fragility fractures, vascular calcification and mortality. There are two main types of vitamin K vitamers: Phylloquinone (or PK) and Menaquinones (MKn). Vitamin K acts both as coenzyme of y-glutamyl carboxylase (GGCX) transforming undercarboxylated in carboxylated vitamin K-dependent proteins (e.g., Osteocalcin and Matrix Gla Protein) and as a ligand of the nuclear steroid and xenobiotic receptor (SXR) (in murine species Pregnane X Receptor: PXR), expressed in osteoblasts. It has been highlighted that the uremic state is a condition of greater vitamin K deficiency than the general population with resulting higher prevalence of bone fractures, vascular calcifications and mortality. The purpose of this literature review is to evaluate the protective role of Vitamin K in bone health in CKD patients.



中文翻译:

CKD 骨病中的维生素 K

维生素 K 主要是已知的,因为它参与血液凝固。此外,流行病学研究表明,其缺陷与脆性骨折、血管钙化和死亡率增加有关。维生素 K 维生素有两种主要类型:叶绿醌(或 PK)和甲基萘醌 (MKn)。维生素 K 既作为 γ-谷氨酰羧化酶 (GGCX) 的辅酶在羧化维生素 K 依赖性蛋白(例如骨钙素和基质 Gla 蛋白)中转化羧基化不足,又作为核类固醇和异生素受体 (SXR) 的配体(在鼠类中) Pregnane X 受体:PXR),在成骨细胞中表达。已经强调,尿毒症状态是一种比一般人群更缺乏维生素 K 的病症,导致骨折、血管钙化和死亡率更高的发生率。

更新日期:2021-01-07
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