Acute and chronic hypoparathyroidism can result in cardiac, renal, and psychiatric disease. Acute treatment consists of intravenous calcium gluconate. The mainstay of chronic treatment consists of calcium and calcitriol. Thiazide diuretics can be used to mitigate calciuria and nephrolithiasis. Calcilytics, which are not yet widely available for treatment of hypoparathyroidism, offer the potential for improved calcium homeostasis and fewer complications, especially to patients with activating CaSR mutations. Hormone replacement therapies such as PTH 1–34 and PTH 1–84 may offer advantages over calcium and calcitriol; however, further studies are required to characterize potential renal protection by reduction of hypercalciuria. Autologous parathyroid transplant is frequently used when risk of hypoparathyroidism is deemed to be high preoperatively or intraoperatively. In general, immediate autotransplant is more successful than transplant after cryopreservation. Conversely, allogeneic parathyroid transplants have not shown long-term success, except in the setting of immunosuppression. Future studies should focus on generation of functional parathyroid cells from autologous sources such as pluripotent stem cells or thymus.