This diminished calcium uptake by bones, together with calcium loading to correct hypocalcemia in a dialysis patient with reduced circulating levels or abnormal variants of mineralization inhibitors, such as Fetuin A or uncarboxylated MGP, are thought to lead to the accumulation of excessive calcium and phosphate deposition in vessels’ walls, particularly within the tunica media and soft tissues [9,21]; however, the exact mechanism is not fully understood. Here, AHSG is linked to Hypocalcemia.