Vitamin K intake and status are low in hemodialysis patients

Ellen C. M. Cranenburg, Leon J. Schurgers, Herma H. Uiterwijk, Joline W. J. Beulens, Gerdien W. Dalmeijer, Ralf Westerhuis, Elke J. Magdeleyns, Marjolein Herfs, Cees Vermeer, Gozewijn D. Laverman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Vitamin K is essential for the activity of gamma-carboxyglutamate (Gla)-proteins including matrix Gla28 protein and osteocalcin; an inhibitor of vascular calcification and a bone matrix protein, respectively. Insufficient vitamin K intake leads to the production of non-carboxylated, inactive proteins and this could contribute to the high risk of vascular calcification in hemodialysis patients. To help resolve this, we measured vitamin K-1 and K-2 intake (4-day food record), and the vitamin K status in 40 hemodialysis patients. The intake was low in these patients (median 140 mu g/day), especially on days of dialysis and the weekend as compared to intakes reported in a reference population of healthy adults (mean K1 and K-2 intake 200 mu g/day and 31 mu g/day, respectively). Non-carboxylated bone and coagulation proteins were found to be elevated in 33 hemodialysis patients, indicating subclinical hepatic vitamin K deficiency. Additionally, very high non-carboxylated matrix Gla28 protein levels, endemic to all patients, suggest vascular vitamin K deficiency. Thus, compared to healthy individuals, hemodialysis patients have a poor overall vitamin K status due to low intake. A randomized controlled trial is needed to test whether vitamin K supplementation reduces the risk of arterial calcification and mortality in hemodialysis patients.
Original languageEnglish
Pages (from-to)605-610
JournalKidney International
Issue number5
Publication statusPublished - Sept 2012


  • hemodialysis hazard
  • mineral metabolism
  • nutrition
  • target organ damage
  • vascular calcification

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