Since mounting evidence points to a central role of a disturbed Wnt–β-catenin signaling in the pathogenesis of CKD-MBD and its cross-talk between the kidneys, the vasculature, and the bone [16], targeting Wnt inhibitors, such as sclerostin or dickkopf1, by monoclonal antibodies would be a potential choice to treat osteoporosis in CKD-MBD. Here, SOST is linked to osteoporosis.