The Role of Vitamin K in Vascular Calcification.

Mario Cozzolino, Maria Fusaro, Paola Ciceri, Lorenzo Gasperoni, Giuseppe Cianciolo

Journal: Advances in chronic kidney disease 2020;26(6):437-444

PMID: 31831122

Abstract

Vascular calcification (VC) is common in advanced chronic kidney disease (CKD), contributes to cardiovascular disease (CVD), and associates with increased mortality. Major risk factors for VC in CKD are increasing age, dialysis vintage, and positive net calcium-phosphate balance. To date, no specific therapy that prevents progression or facilitates regression of VC beyond careful attention to calcium and phosphate balance exists. Accumulating evidence demonstrates that CKD patients may incur subclinical vitamin K deficiency. This deficiency may be induced by exhaustion of vitamin K due to its high requirement by vitamin K-dependent proteins to inhibit VC. This review analyzes the pathophysiological mechanisms and clinical consequences of vitamin K deficiency with emphasis on its involvement on vascular calcification in CKD and end-stage renal disease and its relationship to the bone-vascular axis.

Copyright © 2019 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

Address: Renal Division, ASST Santi Paolo e Carlo, Department of Health Sciences, University of Milan, Milan, Italy. Electronic address: [email protected].; National Research Council (CNR), Institute of Clinical Physiology (IFC), Pisa, Italy; Department of Medicine, University of Padua, Padua, Italy.; Renal Research Laboratory, Department of Nephrology, Dialysis and Renal Transplant, Fondazione Ca' Granda IRCCS, Ospedale Maggiore Policlinico, Milan, Italy.; Nephrology Dialysis and Renal Transplant Unit, Department of Experimental Diagnostic and Specialty Medicine (DIMES), S. Orsola Hospital, University of Bologna, Bologna, Italy.
Bant logo

© Copyright 2026, Nutrition Evidence

NED wishes to thank the following organisations for their support:

We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.