# Vitamin K Status of Patients Undergoing Hemodialysis: Insights from a Cross-Sectional Study
###### Abstract  
(1) Background: Vitamin K deficiency is a common feature of chronic kidney disease (CKD), leading to impaired bone quality and an increased risk of vascular calcifications. A method to indirectly assess the vitamin K status is measuring the blood level of vitamin K-dependent proteins (VKDP): osteoclastcin (OC) and matrix CLA protein (MGP). The aim of this study is to correlate the level of total OC and inactive MGP (dp-uc MGP) with markers of CKD mineral bone disorder (CKD-MBD). (2) Methods: We conducted a single-center cross-sectional study that included 45 CKD GSD patients and measured their blood biochemistry, complete blood count and total osteoclast and dp-uc MGP contents. (3) Results: We found a strong, statistically significant correlation of the total OC with the markers of CKD-MBD, such as: iPTH, serum calcium and serum phosphorus, and a strong, indirect statistically significant correlation with abdominal circumference. There was also a statistically significant correlation of dp-uc MGP with the markers of inflammation (CRP). Higher levels of dp-uc MGP were found in the patients treated with vitamin K antagonists, non-calcium-based phosphate binders and the vitamin D receptor activator, paricalcitol. (4) Conclusions: In our study, we found that when it is measured indirectly using VKDP levels, vitamin K deficiency is associated with CKD-MBD. Certain widely used medications such as phosphate binders reduce vitamin K absorption, supplementary vitamin D increases vitamin K requirements, and also vitamin K antagonists influence the blood level of VKDPs. technodialysis; calcifications; vitamin K; osteoclastcin; matrix Gla protein +
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_Article_  
Vitamin K Status of Patients Undergoing Hemodialysis: Insights from a Cross-Sectional Study  
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1 Deva Emergency County Hospital, 330004 Deva, Romania; [EMAIL_ADDRESS]  
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smoking and age) and non-traditional. The latter ones are represented by factors associated with CKD-associated mineral bone disorder (CKD-MBD), such as high levels of calcium x phosphorus product and fibroblast growth factor 23 (FGF23), and low vitamin D levels or high parathormone levels (PTH) [4], and also inflammation, oxidative stress or uremic toxins. Currently, it is widely accepted that high phosphate levels will trigger the overproduction of FGF23, which acts as a phosphaturic hormone and negatively regulates PTH levels [5]. Despite similar exposure to the risk factors, not all CKD patients develop vascular calcifications. This fact could be explained by the presence of protecting factors in some of the patients, including Fetuin A, Bone morphogenetic protein 7 (BMP 7) and Adenosine, as well as vitamin K [5]. Vitamin K is a fat-soluble vitamine which constitutes the substrate for several vitamin K-dependent proteins (VKDPs), and some of them are involved in the coagulation cascade, cellular adhesion and migration, and bone and vascular homeostasis. The VKDPs implicated in calcification processes are matrix Gla protein (MGP), osteoclast (OC), bone Gla protein, growth arrest-specific protein 6 and Gla-rich protein [6]. Vitamin K deficiency is a frequent concern among CKD patients, particularly patients undergoing hemodialysis (HD) treatment [7]. The underlying mechanism of vitamin K deficiency is a combination between its increased consumption in order to produce vitamin K-dependent calcification inhibiting proteins and reduced vitamin K intake due to low potassium and phosphate diets. Some therapeutic interventions performed for CKD patients have been mentioned to have an impact on vitamin K homeostasis. First of all, we address warfarin-based anticoagulation.