Vitamin K does not appear to improve cardiovascular health in patients with CKD
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Vitamin K supplementation showed no effect on vascular stiffness or other markers of vascular health in patients with chronic kidney disease, according to a randomized controlled trial.
Based on these results, Miles D. Witham, MD, of the National Institute for Health Research Newcastle Biomedical Research Centre in the United Kingdom, and colleagues contended that the therapy may not aid in reducing the risk for cardiovascular disease in this patient population.
“A recent meta-analysis of observational studies confirmed that higher levels of inactive vitamin K-dependent proteins are associated with higher rates of cardiovascular events and death,” the researchers wrote. “Few trials of vitamin K have examined the effect of treatment on vascular calcification or stiffness to date, however, meta-analyses of those that have suggest a potential significant benefit on vascular calcification and a nonsignificant reduction in vascular stiffness.”
They added that although previous studies have demonstrated the importance of vascular calcification as a risk factor for cardiovascular events, only one trial has examined whether vitamin K supplementation can benefit patients with nondialysis-dependent CKD.
To this end, Witham and colleagues randomized 159 patients (mean age, 66 years) to either 1 year of vitamin K2 supplementation (400 mg per day) or placebo. The primary outcome of the study was the between-group difference in pulse wave velocity at 12 months.
“We chose to measure pulse wave velocity rather than directly measuring calcification for several reasons,” they explained. “Any significant change in calcification would be expected to cause a change in arterial stiffness, but pulse wave velocity, as a marker of arterial stiffness, provides not just structural but also functional information on large arteries. It is an independent risk factor for future cardiovascular events and requires fewer participants to demonstrate clinically important treatment effects than measures of vascular calcification.”
Other considered outcomes included augmentation index, abdominal aortic calcification, blood pressure, physical function and blood markers of mineral metabolism and vascular health.
At 12 months, researchers observed no differences in pulse wave velocity between those taking vitamin K vs. placebo. There were also no differences in augmentation index, blood pressure, B-type natriuretic peptide or physical function.
While Witham and colleagues acknowledged that 12 months may not have been a long enough period to produce an observable effect on vascular calcification or on vascular stiffness, they pointed out that strengths of the trial included “the ability to detect a relatively small change in pulse wave velocity, the use of more than one center to recruit participants and the use of a placebo control to ensure masking of outcomes assessments and analyses.”
“Based on our prior assumption that pulse wave velocity is a meaningful surrogate for further cardiovascular events in patients with CKD, our results do not support the hypothesis that administration of vitamin K2 will reduce cardiovascular events in this population,” the researchers concluded. “Combining our results with other recent trials does not currently support the conduct of a large cardiovascular outcome trial using vitamin K2 therapy; instead, alternative methods to improve vascular stiffness in patients with CKD should be explored.”
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