Oral phosphate supplements are currently thought to be the primary intervention to reduce risk for renal mineralization in human carriers of NPT2a and NPT2c mutations. However, there is concern that oral phosphate therapy might contribute to the formation of renal mineralization despite reduced 1,25(OH)2D levels and reduced urinary calcium excretion under certain conditions, for example in patients with X-linked hypophosphatemia (XLH) treated with oral phosphate supplements given multiple times throughout the day [44, 45] and in otherwise healthy individuals following treatment with phosphate enema .