Open AccessVitamin K supplementation and arterial calcification in dialysis: results of the double-blind, randomized, placebo-controlled RenaKvit trial
Author(s) -
Karin Levy-Schousboe,
Marie FrimodtMøller,
Ditte Hansen,
Christian Daugaard Peters,
Krista Dybtved Kjærgaard,
Jens Dam Jensen,
Charlotte Strandhave,
Hanne Elming,
Casper Larsen,
Hanne Sandstrøm,
Claus Lohman Brasen,
Anne Schmedes,
Jonna Skov Madsen,
Niklas Rye Jørgensen,
Jens Brøndum Frøkjær,
Niels Erik Frandsen,
Inge Petersen,
Peter Marckmann
Publication year - 2021
Publication title -
clinical kidney journal
Language(s) - English
Resource type - Journals
eISSN - 2048-8513
pISSN - 2048-8505
DOI - 10.1093/ckj/sfab017
Subject(s) - medicine , matrix gla protein , placebo , calcification , pulse wave velocity , arterial stiffness , gastroenterology , dialysis , vitamin , vitamin d and neurology , randomized controlled trial , peritoneal dialysis , vitamin k2 , endocrinology , surgery , cardiology , blood pressure , pathology , alternative medicine , ectopic calcification
Background Arterial calcification is associated with cardiovascular mortality in dialysis patients. Active matrix Gla protein (MGP) is a vitamin K-dependent inhibitor of arterial calcification. Elevated plasma concentrations of inactive MGP, i.e. dephosphorylated-uncarboxylated MGP (dp-ucMGP), are prevalent in dialysis patients. MGP inactivity might contribute to arterial calcification. We investigated whether vitamin K supplementation had an effect on arterial calcification in chronic dialysis patients. Methods In a 2-year, double-blind, placebo-controlled intervention trial, 48 dialysis patients were randomized to vitamin K [menaquinone-7 (MK-7), 360 µg daily] or placebo. MK-7 in serum and dp-ucMGP in plasma were used to assess vitamin K status. Carotid-femoral pulse wave velocity (cfPWV) and scores of coronary arterial calcification (CAC) and abdominal aortic calcification (AAC) were used to assess arterial calcification. Results Thirty-seven participants completed Year 1, and 21 completed Year 2. At Year 2, serum MK-7 was 40-fold higher, and plasma dp-ucMGP 40% lower after vitamin K supplementation compared with placebo {mean dp-ucMGP difference: −1380 pmol/L [95% confidence interval (CI) −2029 to −730]}. There was no significant effect of vitamin K supplementation on cfPWV [mean difference at Year 2: 1.2 m/s (95% CI −0.1 to 2.4)]. CAC Agatston score increased significantly in vitamin K supplemented participants, but was not significantly different from placebo [mean difference at Year 2: 664 (95% CI −554 to 1881)]. AAC scores increased in both groups, significantly so within the placebo group at Year 1, but with no significant between-group differences. Conclusions Vitamin K supplementation improved vitamin K status, but did not hinder or modify the progression of arterial calcification in dialysis patients.