الفهرس 
SclerostinOnly 14 pages are availabe for public view
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Abstract
Vascular calcification is a common complication in end-stage renal disease (ESRD) on HD, contributing to the high mortality affecting this group. Arterial calcifications are two forms depending on whether it occurs in the intima or media of blood vessels, intimal calcification occurs in the atherosclerotic lesions and medial calcification, which is associated with vascular stiffening and arteriosclerosis. Numerous risk factors have been reported for VCs, some of these are(classic), as aging, hypertension, diabetes and dyslipidaemia; certain others are more specific to CKD and are (non-traditional), such as mineral metabolism abnormalities, particularly hyperphosphataemia and extreme PTH serum levels, dialysis duration and excess administration of calcium salts. Sclerostin, the protein product of the SOST gene, is an osteocyte product that functions as a soluble antagonist of the Wnt/β-catenin signalling and profoundly influences bone metabolism. The main action of sclerostin is a decrease in bone formation and that sclerostin is up-regulated in the vascular wall during the vascular calcification process, it may be hypothesized that sclerostin is part of a local counter regulatory mechanism directed to suppress VC. Sclerostin produced in the vascular wall may spill over to the circulation and thereby contribute to circulating levels of the protein.