Journal
CURRENT OSTEOPOROSIS REPORTS
Volume 20, Issue 1, Pages 65-77Publisher
SPRINGER
DOI: 10.1007/s11914-022-00716-z
Keywords
Vitamin K; Chronic kidney disease; Inflammation; Cardiovascular disease; Bone fractures
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This review discusses the mechanism of action of vitamin K and its implications in cardiovascular disease, bone fractures, and inflammation. It highlights the protective role of vitamin K, especially in chronic kidney disease (CKD), and emphasizes the importance of vitamin K dosage in reducing bone fractures and improving vascular calcifications.
Purpose of Review We describe the mechanism of action of vitamin K, and its implication in cardiovascular disease, bone fractures, and inflammation to underline its protective role, especially in chronic kidney disease (CKD). Recent Findings Vitamin K acts as a coenzyme of y-glutamyl carboxylase, transforming undercarboxylated in carboxylated vitamin K-dependent proteins. Furthermore, through the binding of the nuclear steroid and xenobiotic receptor, it activates the expression of genes that encode proteins involved in the maintenance of bone quality and bone remodeling. There are three main types of K vitamers: phylloquinone, menaquinones, and menadione. CKD patients, for several conditions typical of the disease, are characterized by lower levels of vitamin K than the general populations, with a resulting higher prevalence of bone fractures, vascular calcifications, and mortality. Therefore, the definition of vitamin K dosage is an important issue, potentially leading to reduced bone fractures and improved vascular calcifications in the general population and CKD patients.
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