Abstract
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.
Highlights
Vascular calcification (VC) represents an independent risk factor for cardiovascular disease in hemodialysis patients [1]
There were no significant changes in carotid intimal medial thickness (CIMT) and aorta calcification score (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
There was a significant increase in Matrix Gla protein (MGP) levels in the Vitamin K group (75.7±26 ng/mL) after vitamin K supplementation compared to its baseline levels (51.49±12 ng/mL)
Summary
Vascular calcification (VC) represents an independent risk factor for cardiovascular disease in hemodialysis patients [1]. Classical atherosclerotic endpoints such as stroke or myocardial infarction are the dominant cause of death. CKD patients mostly die from sudden cardiac death or ischemic heart disease due to premature vascular and cardiac aging [2]. Vascular calcification is highly prevalent in ESKD and independently predictive of future cardiovascular events and mortality [3]. Calcification can occur in both the intimal and medial layers of vasculature, but medial calcification is the major form in ESKD. Medial calcification increases large elastic artery stiffness and pulse-pressure, promotes left ventricular hypertrophy, reduces perfusion of the coronary arteries, and promotes increased cardiovascular mortality via increased risk of myocardial infarction and heart failure [3]
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