Calcified vessels on bone turnover in chronic kidney disease (CKD). The phenotypic osteoblast/osteocyte in calcified vessels may secrete sclerostin (SOST), secreted frizzled-related protein (sFRP), and Dickkopf-related protein 1 (DKK1), which prevent further calcification of the affected vessel. The secreted SOST and sFRP will process autocrine or paracrine effects to inhibit Wnt signaling effects on osteogenic transdifferentiation of VSMCs, which will prevent further calcification of the vessel wall. As the SOST and sFRP secreted from calcified vessel are released into circulation, they may inhibit Wnt signaling in osteoblast in the bone. This inhibition of bone osteoblasts reduces bone accretion and turnover, resulting in a fragile bone, which may also contribute elevated serum inorganic phosphates. In addition, DKK1 enhances RANKL levels, and the increased RANKL : OPG ratio activates osteoclast activity, leading to the increase of bone resorption.