These seemingly contradictory findings could reflect a number of pathological mechanisms: (1) sclerostin inhibits osteoblastic differentiation in bone but not osteoblastic transdifferentiation in the vessels; (2) sclerostin-induced decrease in bone turnover may lead to higher circulating calcium and phosphorus levels that stimulate vascular calcification; (3) there might be a shift in the source of sclerostin production in CKD. Here, SOST is linked to chronic kidney disease.