الفهرس 
Introduction
Bone and KidneyOnly 14 pages are availabe for public view
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Abstract
Sclerostin is a negative regulator of bone formation that is expressed exclusively in osteocytes of mouse and human bone and suppresses bone formation by inhibiting the differentiation of osteoblasts. Sclerostin may play an important role in CKD-MBD.
The aim of our cross-sectional study is to study the correlation between circulating sclerostin levels and bone mineral density, and vascular calcifications; and to test if there is any correlation between sclerostin levels and the underlying etiology of CKD.
40 HD patients (aged 41.12 14.2years) were recruited from a Minia University Hospital dialysis center as well as 20 age- and sex-matched healthy controls (aged 40.4 13.94) participated in this study. Circulating sclerostin levels, 25, (OH)2 D, and iPTH were measured. High resolution peripheral quantitative computed tomography (HR-pQCT) was used to measure bone mineral density. MDCT scan was used to detect vascular calcification along the whole course of aorta. Transthoracic echocardiography was used to detect vascular calcifications.
The mean sclerostin level was 1.5-fold higher in dialysis patients than in healthy controls. Sclerostin was negatively associated with duration of dialysis (R -0.365, p < 0.021). Sclerostin levels were significantly positively correlated with bone mineral density and microarchitecture (R 0.697, p < 0.001). The mean serum sclerostin levels is significantly lower in hemodialysis patients with vascular calcification (p = 0.028). The mean sclerostin level was higher in dialysis patients secondary to glomerulonephritis as compared to other etiologies.
In conclusion we found that higher sclerostin levels were associated with better bone density and microarchitecture, and lesser vascular calcification in hemodialysis patients. Moreover, circulating sclerostin levels show a trend to be higher in dialysis patients secondary to glomerulonephritis.
Our study in addition to a similar study should spark interest into research aimed at further elucidating additional mechanisms by which sclerostin affect bone turnover and cardiovascular calcification in hemodialysis patients; and whether these findings are also working in CKD stages 3-4.