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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). 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. © 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Citation

Maria Fusaro, Francesco Tondolo, Lorenzo Gasperoni, Giovanni Tripepi, Mario Plebani, Martina Zaninotto, Thomas L Nickolas, Markus Ketteler, Andrea Aghi, Cristina Politi, Gaetano La Manna, Maria Luisa Brandi, Serge Ferrari, Maurizio Gallieni, Maria Cristina Mereu, Giuseppe Cianciolo. The Role of Vitamin K in CKD-MBD. Current osteoporosis reports. 2022 Feb;20(1):65-77

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PMID: 35132525

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