Regression of uremic tumoral calcinosis following the switch from cinacalcet to etelcalcetide in a hemodialysis patient without severe hyperphosphatemia.

Tumoral calcinosis (TC), a rare disease characterized by calcified mass formation in peri-articular soft tissue, manifests clinically as fractures, pain, and limited range of motion. In hemodialysis patients, severe hypercalcemia and hyperphosphatemia are major causes of the condition, and correcting these metabolic disorders reportedly induces its regression. Herein, we report the case of a 46-year-old man on maintenance hemodialysis who developed TC that regressed following etelcalcetide therapy despite the absence of severe hyperphosphatemia. The patient had started hemodialysis at age 32, and soft tissue calcifications were first noted two years later. These progressed to TC, which caused a left femoral shaft fracture 13 years after the initiation of dialysis. When the fracture occurred, TC was present in both thighs and the left elbow. Seven months after the fracture, he was referred to our department. Laboratory findings showed serum phosphate, corrected calcium, and intact parathyroid hormone levels of 4.9 mg/dL, 10.3 mg/dL, and 109 pg/mL, respectively. Cinacalcet was switched to intravenous etelcalcetide hydrochloride, and significant regression of the remaining TC was observed six months after the switch. Our findings suggest that etelcalcetide may be effective for TC in patients on hemodialysis, even in the absence of severe hypercalcemia or hyperphosphatemia. However, further reports are required to determine whether this observation is generalizable.