الفهرس 
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Abstract
Cardiovascular calcification is a risk factor and contributor to morbidity and mortality in End stage kidney disease patients. Cardiovascular calcification is most likely due to an imbalance of promoters (e.g. Calcium and phosphate) and inhibitors (e.g. fetuin-A and matrix Gla protein) (Schlieper et al., 2015).
Vitamin K functions as an enzyme cofactor for the carboxylation of vitamin K–dependent proteins involved in many physiological processes, including vascular calcification. Although various vitamin K–dependent proteins have been identified in vascular tissue and have also been implicated in arterial calcification and CVD, the most studied is matrix gla protein (MGP) (Tesfamariam 2019).
We aimed to study the effect of oral vitamin k2 on serum carboxylated Matrix gla protein in patients on maintenance hemodialysis and to study its effect as an important marker of vascular calcification.
This Placebo Controlled clinical trial was conducted for 3 months on 80 adult ESRD patients on regular Hemodialysis randomly allocated into 2 groups of either vitamin K2 versus oral placebo tablet administration for 3 months.
Patients in both groups were age and sex matched, study group included 20 (50%) males and 20 (50%) females with mean age ± SD (46.200 ± 14.730) years and 16 (40%) males and 24 (60%) females in the placebo group with mean age ± SD 49.500 ± 14.509 years. with no significant difference between both groups as regard demographic data, access of hemodialysis, and duration of Hemodialysis.
There was no significant change in bone parameters (serum Ca, PO4 & Ca/PO4 product) after 3 months of vit K2 administration compared to baseline in the study group.
Serum phosphorus levels showed a minimal, yet statistically significant decrease after 3 months of placebo administration, this might be attributed to the different doses of PO4 binders in patients of both groups.
Consequently, Ca/ PO4 product showed a statistically significant decrease after 3 months of placebo administration (P=0.002), mostly attributed to the significant decrease in serum phosphorus in the same group over the same period.
We observed that serum MGP levels significantly increased after administration of vitamin k2 in study group (P<0.001) with714.52% increase. However, a much lower increase, yet statistically significant increase in serum MGP level was noticed in the placebo group (P<0.001) with 40.60 % increase.
There was no statistically significant difference between the two groups according to their risk factors regarding smoking, HTN, HCV, DM, and ISHD.
Age has an insignificant effect on MGP level neither in the study group at baseline or after 3 months of vit K2 therapy (P=0.710, P=0.616) respectively, nor in the placebo group at baseline or after placebo administration for 3 months (P=0.841, 0.332) respectively.
The current study showed that duration of hemodialysis has no effect in the study group.
Different risk factors including Hypertension, Diabetes Mellitus, Smoking, Heart failure, Ischemic heart disease and hepatitis c virus has no significant effect on serum MGP levels neither before nor after therapy in both study and placebo groups.
We concluded that Oral vitamin K2 therapy significantly increased serum active form of Matrix GLA protein levels among hemodialysis patients with potential decrease in cardiovascular calcification and cardiovascular diseases.
Limitations of the study are the relatively small sample size, with no funding present. Serum levels of vitamin k2 was not measured before or after therapy, also no imaging was done to assess the effect of vitamin k2 administration and rise in serum MGP level on vascular calcification.