Secondary hyperparathyroidism (SHPT) is a major problem in chronic kidney disease (CKD), as it is associated with greater bone turnover and increased risks of fractures and cardiovascular mortality. The clinical use of calcimimetics, which improve the sensitivity of the calcium‒sensing receptor, has markedly facilitated the treatment of SHPT. However, here we report three hemodialysis‒dependent cases of hypercalcemia caused by the inappropriate use of the second‒generation calcimimetic etelcalcetide under low bone turnover. The serum calcium levels of a 38‒year‒old male, 62‒year‒old male, and 66‒year‒old female continued to increase to＞12 mg/dL in the presence of low serum intact parathyroid hormone levels (≤21 pg/mL), even after the discontinuation of oral or intravenous active vitamin D analogs. The patients’ serum calcium levels normalized about a month after the discontinuation of intravenous etelcalcetide. The administration of etelcalcetide under low bone turnover presumably caused adynamic bone disease and reduced the buffering capacity of calcium, resulting in hypercalcemia. Understanding the pathophysiology of bone disease and the appropriate use of calcimimetics are necessary in CKD patients.