Chronic renal disease is a worldwide major health problem, with increasing incidence, prevalence, high costs, and poor outcomes. 1 Mortality among patients with CKD and ESRD remains high due to its association with the occurrence of ischemic heart disease (IHD). 2 Numerous data show a close relationship between inflammation and cardiovascular morbidity and mortality. Hs-CRP is an important indicator and diagnostic tool for systemic inflammation. It has been found that Interleukin-6 and tumour necrosis factor-α are proinflammatory cytokines that can stimulate CRP synthesis in the liver. 3 All these biomarkers are very useful in the prediction of cardiovascular complications and mortality in ESRD patients. 4 Renal function impairment frequently leads to IHD. There are many traditional risk factors associated with IHD. Nowadays non-traditional CKD-specific risk factors for IHD appeared. Among the most important non-conventional risk factors are uremic toxins (UTs). Despite many studies either

Introduction: Matrix Gla protein (MGP) is a central calcification inhibitor of vascular wall. The biological activation of the calcification-inhibitory protein MGP can be achieved by simple administration of oral vitamin K. Aim: The study was conducted to assess the effect of vitamin k supplementation on vascular calcification and to evaluate its effect on MGA in hemodialysis patients. Materials and Methods: Forty adult patients with end stage renal disease (ESRD) on regular hemodialysis sessions, thrice weekly, were enrolled in the study and were randomly assigned into two groups. Vitamin K group consisted of 20 patients were given oral vitamin K at 10 mg after each session of dialysis for a duration of one year. No-Vitamin K group included 20 patients didn’t receive vitamin K. All patients were subjected to the following: Matrix Gla protein (MGP), in addition to, plain digital abdominal x-ray and doppler ultrasound. Results: After one-year of vitamin K supplementation, a significant increase in MGP levels in Vitamin K group (75.7±26 ng/mL) were noticed. There were no significant changes in CIMT and AACS in Vitamin K group after vitamin K supplementation in compared to their baseline levels, while the CIMT and AACS were significantly increased in No-Vitamin K group in compared to their baseline levels. Conclusion: Vitamin K supplementation could not stop vascular calcifications but significantly attenuate their progression.