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Abstract: PO2547

Vitamin K1 Retards Progression of Cardiovascular Calcifications in Hemodialysis Patients: The VitaVasK Trial

Session Information

Category: Hypertension and CVD

  • 1402 Hypertension and CVD: Clinical, Outcomes, and Trials


  • Saritas, Turgay, University Hospital RWTH Aachen, Aachen, Germany
  • Reinartz, Sebastian Daniel, University Hospital RWTH Aachen, Aachen, Germany
  • Krueger, Thilo, DaVita, Geilenkirchen, Germany
  • Evenepoel, Pieter, University Hospitals Leuven, Leuven, Belgium
  • Jadoul, Michel Y., Cliniques Saint-Luc, University of Louvain Medical School, Brussels, Belgium
  • Kopp, Christoph, Universitatsklinikum Erlangen, Erlangen, Bayern, Germany
  • Ketteler, Markus, Robert-Bosch-Krankenhaus GmbH, Stuttgart, Baden-Württemberg, Germany
  • Stenvinkel, Peter, Karolinska Universitetsjukhuset i Huddinge, Huddinge, Sweden
  • Westenfeld, Ralf, Heinrich-Heine-Universitat Dusseldorf, Dusseldorf, Nordrhein-Westfalen, Germany
  • Wied, Stephanie, University Hospital RWTH Aachen, Aachen, Germany
  • Siepmann, Robert, University Hospital RWTH Aachen, Aachen, Germany
  • Hilgers, Ralf-dieter, University Hospital RWTH Aachen, Aachen, Germany
  • Schurgers, Leon J., Universiteit Maastricht, Maastricht, Limburg, Netherlands
  • Floege, Jürgen, University Hospital RWTH Aachen, Aachen, Germany

Cardiovascular calcifications are prevented by matrix Gla protein (MGP), a protein activated by vitamin K. As HD patients exhibit marked vitamin K deficiency, the VitaVasK trial (EudraCT No.: 2010-021264-14) analysed whether vitamin K1 supplementation affects progression of coronary artery calcifications (CAC) and thoracic aortic calcifications (TAC) in these patients.


This prospective, open-label, multicenter trial randomized patients with preexisting CAC to continue on standard care or to additionally receive 5 mg vit K1 orally thrice weekly. Primary end points were progression of TAC and CAC volume scores in CT scans during 18 months. Repeated linear mixed effects models assessed the treatment effect after adjusting for study site.


Of 60 randomized patients, 20 dropped out for reasons unrelated to vit K1, resulting in 23 control and 17 vit K1 patients. The trial was stopped early due to low recruitment rate. TAC progressed significantly between baseline and 18 months but its progression was reduced by a mean of 56% in the vit K1 compared to the control group at 18 months (p=0.039) (Table). CAC significantly progressed within the control group, but not within the vit K1 group. Progression at 18 months was lower by an average of 68% in the vit K1 group compared to the control group (p=0.072). Inactive dp-ucMGP in plasma was elevated at baseline, confirming vit K deficiency. Levels at 18 months were 110±40% of baseline in controls but rapidly dropped in the vit K1 group to 27±12% at 18 months. No treatment-related adverse events were noted.


Despite early termination, this randomized trial identifies a highly effective mode of correcting the vit K deficiency in chronic HD patients. Our intervention is potent, safe and cost-effective to reduce progression of cardiovascular calcification in this high-risk population.

: Changes in volume score versus baseline within groups
 Thoracic aortaCoronary arteries
Vitamin K1Baseline vs. 12 months479 (256), 0.0668142 (138), 0.3092
Baseline vs. 18 months710 (323), 0.0318197 (169), 0.2505
ControlBaseline vs. 12 months805 (214), 0.0004408 (116), 0.0009
Baseline vs. 18 months1601 (274),*<0.0001
609 (149), 0.0001

Data are means (SE), adjusted for study site, and p-value. * p<0.05 versus vitamin K1


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