Vascular calcification occurs when
calcium accumulates in the intima (associated with
atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the
calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts
cardiovascular disease (CVD) and mortality. A preventive role for
vitamin K in
vascular calcification has been proposed based on its role in activating
matrix Gla protein (MGP), a calcification inhibitor that is expressed in vascular tissue. Although animal and in vitro data support this role of
vitamin K, overall data from human studies are inconsistent. The majority of population-based studies have relied on
vitamin K intake to measure status.
Phylloquinone is the primary dietary form of
vitamin K and available supplementation trials, albeit limited, suggest
phylloquinone supplementation is relevant to CAC. Yet observational studies have found higher dietary
menaquinone, but not
phylloquinone, to be associated with less calcification.
Vascular calcification is highly prevalent in certain patient populations, especially in those with
chronic kidney disease (CKD), and it is plausible
vitamin K may contribute to reducing
vascular calcification in patients at higher risk. Subclinical
vitamin K deficiency has been reported in CKD patients, but studies linking
vitamin K status to calcification outcomes in CKD are needed to clarify whether or not improving
vitamin K status is associated with improved vascular health in CKD. This review summarizes the available evidence of
vitamin K and
vascular calcification in population-based studies and clinic-based studies, with a specific focus on CKD patients.