Although the pathogenesis of AKI owing to hypercalcemia is not fully understood, the following mechanisms have been reported: (1) circulating volume depletion occurs as a result of hypercalcemia, causing impaired renal concentrating capacity due to inhibition of sodium and chloride reabsorption in the ascending limb of Henle’s loop and a reduced response of antidiuretic hormone in collecting ducts20,21; (2) direct renal vasoconstrictive effects due to hypercalcemia22; and (3) tubulointerstitial injury due to calcium deposition23,24. The gene discussed is AVP; the disease is Hypercalcemia.