# Vitamin K Status of Patients Undergoing Hemodialysis: Insights from a Cross-Sectional Study
## 4 Discussion  
In recent years, the central role of vitamin K in vascular calcifications, cardiovascular issues and bone disease has become evident. Several studies have been performed assessing the link between vitamin K metabolism and mineral bone disease in CKD patients. CKD patients, and especially patients treated with hemodialysis, are vitamin K-deficient. In a study performed by [PERSON] et al., it was shown that dialysis patients were 100% vitamin K-deficient, not due to HD wash-out or absorption capacity [16], but due to low vitamin K intake. Low vitamin K intake could be due to potassium-sparing diets which restrict the consumption of leafy greens rich in vitamin K. The assessment of vitamin K status can be performed using the levels of fragments of VKDP, or the ratio between the fragments and total VKDP. However, in patients treated with HD, the use of these ratios might negate their significance as a bone metabolic marker to indicate vitamin K deficiency [17]. In our study, we have used the total OC and dp-uc MGP, and we found higher levels compared to the normal ranges, which is a fact that might lead to the conclusion of vitamin K deficiency. The consequences of vitamin K deficiency are mainly related to CKD-MBD. In the present study, we obtained a significant correlation between the total OC and the markers of CKD-MBD. OC is secreted in bones by osteoblasts and plays a role in the synthesis and regulation of the bone matrix [6]. The previous literature results focus on the relationship between fragments of OC (undercarboxylated OC) and PTH and calcium phosphorus products [18]. However, our study confirmed the direct relationship between these markers of CKD-MBD and the total OC as well. Regarding dp-uc MGP, we found no statistically significant correlation with the markers of CKD-MBD. In contrast to our observations, [PERSON] et al. [19] found significant associations between these MGP fragments and serum PTH, FGF23 levels and calcium phosphorus products. The clinical link between poor vitamin K status and bone health has also been proven in clinical studies assessing the incidence of fractures in CKD patients [20], with vitamin K1 deficiency being the strongest predictor of vertebral fractures [21]. In our study, we could not find any statistical correlation between vitamin K status assessed by dp-uc MGP and total OC and bone fractures because of the low number of patients with a history of fractures (two patients). Another key point assessed in our study was the relationship between VKDP and malnutrition as well as inflammation. It seems that vitamin K plays a key role in counteracting inflammation, oxidative stress and senescence. The link between malnutrition and arterial calcifications in patients treated with HD has been studied by [PERSON] et al. [22]. The study included 68 chronic patients undergoing HD, and they learned that MGP immunostaining in calcified radial arteries positively correlates with calcium x phosphorus product, albumin, and with the modified quantitative subjective global assessment. In our study, we did find a significant correlation between the inflammatory markers, CRP and VKDP (dp-uc MGP). Persistent, low-grade inflammation is a novel non-traditional risk factor for accelerated atherosclerosis, either on its own, or included in the Malnutrition Inflammation Atherosclerosis Syndrome. Even though the molecular pathway through which vitamin K is involved in oxidative stress, DNA repairing and inflammation is well known, the relationship between inflammatory markers and vitamin K in patients undergoing HD has not been extensively studied. Since vitamin K is known to be a protective factor against vascular calcifications, another consequence of vitamin K deficiency is the fact that it contributes to the high burden of vascular calcifications in CKD patients.