Abstract

Purpose Functional vitamin K deficiency (both K1 and K2) is postulated to be one of the most relevant links between chronic kidney disease and vascular calcification in hemodialysis (HD) patients. Recommended dietary restrictions in HD patients superimposed on diversity of eating habits across the countries may affect the prevalence of functional vitamin K deficiency. The aim of this study was to determine the level of functional vitamin K deficiency and its relation to vitamin K1 intake in HD patients in Upper Silesia in Poland.MethodsProtein-induced vitamin K absence or antagonist-II (PIVKA-II) and undercarboxylated matrix Gla protein (ucMGP) were assessed by ELISA in 153 stable, prevalent HD patients and 20 apparently healthy adults (to establish normal ranges for PIVKA-II and ucMGP). Daily phylloquinone intake was assessed using a food frequency questionnaire.ResultsPIVKA-II and ucMGP levels were increased in 27.5 and 77.1 % of HD patients in comparison with the reference ranges in apparently healthy controls, respectively. In 45 % of cases, the increased PIVKA-II level was explained by insufficient phylloquinone intake for Polish population (recommended intake: >55 μg for women and >65 µg for men). Applying ROC analysis, we showed that vitamin K1 intake below 40.2 µg/day was associated with increased PIVKA-II levels. There was no correlation between vitamin K1 intake and plasma concentration of ucMGP, or between PIVKA-II and ucMGP. Conclusions(1) Functional vitamin K1 deficiency is explained by low vitamin K1 intake in less than half of HD patients. (2) Undercarboxylated matrix Gla protein level is a poor surrogate for functional vitamin K1 deficiency.

Highlights

  • Cardiovascular diseases are the main causes of morbidity and mortality in patients with chronic kidney disease (CKD)

  • The results of our study increase the knowledge concerning the regional variability of the prevalence of functional vitamin K deficiency in HD patients and indicate the need for the standardization of methods used for its assessment

  • A recent study by Holden and co-workers in 172 subjects with stage 3–5 CKD showed that the criteria for subclinical vitamin K deficiency were met by 6 % of the patients based on circulating K1 measurements, by 60 % based on OC carboxylation and by 97 % based on PIVKA-II levels [9]

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Summary

Introduction

Cardiovascular diseases (coronary artery disease, congestive heart failure, arrhythmias or sudden cardiac death) are the main causes of morbidity and mortality in patients with chronic kidney disease (CKD). Increased mortality in hemodialysis (HD) patients often is associated with accelerated atherosclerosis and excessive vascular calcification [1]. Increased risk of the development of cardiovascular calcification in patients with CKD can only partly be explained by the presence of established risk factors such dyslipidemia, hypertension, smoking habit or diabetes [2, 3]. Functional deficiency of proteins involved in the regulation of calcium metabolism is probably a crucial mechanism for this process [2]. The term ‘vitamin K’ refers to a group of compounds consisting of the plant form, phylloquinone (vitamin K1), the bacterial form, the menaquinones (MK, vitamin K2) and a synthetic form, menadione (vitamin K3), which is an intermediate in vitamin K metabolism [8]

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