Abstract
Chronic kidney disease (CKD) patients have a higher risk of cardiovascular (CVD) morbidity and mortality compared to the general population. The links between CKD and CVD are not fully elucidated but encompass both traditional and uremic-related risk factors. The term CKD-mineral and bone disorder (CKD-MBD) indicates a systemic disorder characterized by abnormal levels of calcium, phosphate, PTH and FGF-23, along with vitamin D deficiency, decreased bone mineral density or altered bone turnover and vascular calcification. A growing body of evidence shows that CKD patients can be affected by subclinical vitamin K deficiency; this has led to identifying such a condition as a potential therapeutic target given the specific role of Vitamin K in metabolism of several proteins involved in bone and vascular health. In other words, we can hypothesize that vitamin K deficiency is the common pathogenetic link between impaired bone mineralization and vascular calcification. However, some of the most common approaches to CKD, such as (1) low vitamin K intake due to nutritional restrictions, (2) warfarin treatment, (3) VDRA and calcimimetics, and (4) phosphate binders, may instead have the opposite effects on vitamin K metabolism and storage in CKD patients.
Highlights
Cardiovascular (CV) disease is the most common cause of morbidity and mortality in patients with chronic kidney disease (CKD) [1,2].The high CV risk may be due, at least in part, to the excess of vascular calcifications (VC) observed even in very young dialysis patients, who lack the typical CV risk factors such as hypertension, dyslipidemia, and smoking [3,4,5]
Chronic kidney disease–mineral bone disorder (CKD-MBD) is considered one of the main factors associated with increased cardiovascular morbidity
As a growing body of evidence has seemed to point to an involvement of vitamin K deficiency in VC, the hypothesis that vitamin K supplementation could be a tool to prevent the rapid progression of VC in CKD patients is gaining momentum [14]
Summary
Cardiovascular (CV) disease is the most common cause of morbidity and mortality in patients with chronic kidney disease (CKD) [1,2]. Chronic kidney disease–mineral bone disorder (CKD-MBD) is considered one of the main factors associated with increased cardiovascular morbidity. Nutrients 2020, 12, 1609 and mortality in CKD patients [11] These patients frequently show both impaired bone mineralization and ectopic vessel mineralization, a feature which is the result of at least two factors: the “bone–vessel axis” and the “calcification paradox”. Treatments targeting bone disorders might have adverse consequences for cardiovascular health This creates the need to identify treatments that have a positive impact on the factors or pathways involved in the crosstalk between vasculature and bone. As a growing body of evidence has seemed to point to an involvement of vitamin K deficiency in VC, the hypothesis that vitamin K supplementation could be a tool to prevent the rapid progression of VC in CKD patients is gaining momentum [14]
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