Meeting News

Vitamin K status shows no impact on progression of vascular calcification in hemodialysis

Rogier Caluwe

WASHINGTON — After stopping therapy with vitamin K antagonists, patients with atrial fibrillation who received rivaroxaban plus vitamin K2 saw improvements in vitamin K status, according to data presented at ASN Kidney Week. However, no beneficial impact on vascular calcification was observed.

“Vitamin K antagonists, although commonly used to reduce thromboembolic risk in atrial fibrillation, have been incriminated as a probable cause of accelerated vascular calcification in hemodialysis patients,” Rogier Caluwe, MD, FASN, a nephrologist at OLV Hospital in Belgium, and colleagues wrote in a poster abstract. “Functional vitamin K deficiency may further contribute to their susceptibility for vascular calcification.”

In an on-site interview, Caluwe told Healio Nephrology that “as clinical nephrologists, we are confronted every day with the consequences of vascular calcification in dialysis patients.”

To investigate the effect of vitamin K status on vascular calcification, researchers randomized 132 patients with atrial fibrillation to 10 mg of rivaroxaban daily, 10 mg of rivaroxaban daily plus vitamin K2 or vitamin K antagonist.

They found the initiation or continuation of vitamin K antagonist therapy further increased desphospho-uncarboxylated Matrix Gla-Protein. While levels decreased in both rivaroxaban groups (larger decreases with vitamin K2), the levels remained elevated.

No substantial differences were observed between groups regarding coronary artery, thoracic aorta and cardiac valve calcium scores or pulse wave velocity. Outcomes of mortality, stroke, cardiovascular event rates and bleeding episodes were also similar between groups (though incidence of life-threatening and major bleeding was lower for those taking rivaroxaban than vitamin K antagonists).

Caluwe said that, despite the results of this trial, vitamin K should still be considered as an approach to protect patients with kidney disease against vascular decalcification and interventions should be started at earlier stages.

However, he argued, “it’s too early to advocate the use of vitamin K supplements at the moment. We need more data.” For these data, he anticipates the results of the vitamin K1 to slow vascular calcification in hemodialysis patients trial, also known as VitaVasK, which will be available next year. – by Melissa J. Webb

Reference:

de Vriese AS, et al. Abstract TH-PO1193. Presented at: ASN Kidney Week; Nov. 7-10, 2019; Washington, D.C.

Disclosure: Caluwe reports no relevant financial disclosures.

 

 

Rogier Caluwe

WASHINGTON — After stopping therapy with vitamin K antagonists, patients with atrial fibrillation who received rivaroxaban plus vitamin K2 saw improvements in vitamin K status, according to data presented at ASN Kidney Week. However, no beneficial impact on vascular calcification was observed.

“Vitamin K antagonists, although commonly used to reduce thromboembolic risk in atrial fibrillation, have been incriminated as a probable cause of accelerated vascular calcification in hemodialysis patients,” Rogier Caluwe, MD, FASN, a nephrologist at OLV Hospital in Belgium, and colleagues wrote in a poster abstract. “Functional vitamin K deficiency may further contribute to their susceptibility for vascular calcification.”

In an on-site interview, Caluwe told Healio Nephrology that “as clinical nephrologists, we are confronted every day with the consequences of vascular calcification in dialysis patients.”

To investigate the effect of vitamin K status on vascular calcification, researchers randomized 132 patients with atrial fibrillation to 10 mg of rivaroxaban daily, 10 mg of rivaroxaban daily plus vitamin K2 or vitamin K antagonist.

They found the initiation or continuation of vitamin K antagonist therapy further increased desphospho-uncarboxylated Matrix Gla-Protein. While levels decreased in both rivaroxaban groups (larger decreases with vitamin K2), the levels remained elevated.

No substantial differences were observed between groups regarding coronary artery, thoracic aorta and cardiac valve calcium scores or pulse wave velocity. Outcomes of mortality, stroke, cardiovascular event rates and bleeding episodes were also similar between groups (though incidence of life-threatening and major bleeding was lower for those taking rivaroxaban than vitamin K antagonists).

Caluwe said that, despite the results of this trial, vitamin K should still be considered as an approach to protect patients with kidney disease against vascular decalcification and interventions should be started at earlier stages.

However, he argued, “it’s too early to advocate the use of vitamin K supplements at the moment. We need more data.” For these data, he anticipates the results of the vitamin K1 to slow vascular calcification in hemodialysis patients trial, also known as VitaVasK, which will be available next year. – by Melissa J. Webb

Reference:

de Vriese AS, et al. Abstract TH-PO1193. Presented at: ASN Kidney Week; Nov. 7-10, 2019; Washington, D.C.

Disclosure: Caluwe reports no relevant financial disclosures.

 

 

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