Vitamin K1 and progression of cardiovascular calcifications in hemodialysis patients: the VitaVasK randomized controlled trial
What this study found
Vitamin K1 reduced progression of vascular calcification overall, with the clearest benefit seen for thoracic aortic calcification. At 18 months, TAC progression was lower with Vitamin K1 versus control by 892.1 (SE 423.0), P = .039; CAC progression showed a favorable but not statistically significant trend, 412.7 (SE 225.4), P = .072. The Agatston secondary analysis also favored Vitamin K1, with an average reduction of 565.8 (SE 252.0), P = .028. Vitamin K1 increased circulating vitamin K levels by +590% at 18 months and reduced dp-ucMGP, consistent with vitamin K repletion; no major safety…
- Study & population
- Open-label randomized controlled trial with assessor-blinded outcome assessment across four sites in Germany, two in Belgium, and one in Sweden.
- Intervention
- Vitamin K1 was given as 5 mg orally thrice weekly during hemodialysis, using liquid vitamin K1 10 mg/ml (Ka-Vit), in addition to usual standard care for 18 months.
- Key limitation
- The trial was stopped early because of slow recruitment, leaving a small analyzed Vitamin K1 sample (n = 17).
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Open PDFOriginal abstract
Abstract Background Cardiovascular calcifications are prevented by matrix Gla protein (MGP), a vitamin K–dependent protein. Haemodialysis patients exhibit marked vitamin K deficiency. The randomized, prospective, open-label, multicentre VitaVasK trial analysed whether vitamin K1 supplementation reduces progression of coronary artery calcifications (CACs) and thoracic aortic calcifications (TACs). Methods Patients with pre-existing CACs were randomized to continue on standard care or to additionally receive 5 mg of vitamin K1 orally thrice weekly. Hierarchically ordered primary endpoints were progression of TAC and CAC in computed tomography scans at 18 months. Linear mixed effects models with repeated measures at baseline and 12 and 18 months assessed treatment effects after adjusting for study site. Results Of 60 randomized patients, 20 dropped out for reasons unrelated to vitamin K1, resulting in 23 control and 17 vitamin K1 patients. The trial was stopped early due to slow recruitment. At 18 months, the average TAC progression was 56% lower in the vitamin K1 compared with the control group (p = .039). CAC significantly progressed within the control group, but not within the vitamin K1 group. Average progression at 18 months was 68% lower in the vitamin K1 compared to the control group (P = .072). Vitamin K1 reduced plasma levels of pro-calcific uncarboxylated MGP by 69% at 18 months. No treatment-related adverse events were noted. Conclusion Vitamin K1 intervention is a potent, safe and cost-effective approach to correct vitamin K deficiency and to potentially reduce cardiovascular calcification in this high-risk population.