Regression of Tumoral Calcinosis After the Appropriate Control of a Deranged Mineral and Bone Metabolism, in Conjugation With Cinacalcet Hydrochloride Treatment, in a Chronic Hemodialysis Patient

Dear Editor, Uremic tumoral calcinosis is an ectopic calcification that is frequently associated with persistent hypercalcemia and hyperphosphatemia in dialysis patients (1). In recent years, calcimimetic compounds have become widely used in dialysis patients for controlling secondary hyperparathyroidism (SHPT). Because cinacalcet can lower the serum parathyroid hormone (PTH),calcium (Ca),and phosphorus (P) levels simultaneously, it can therefore potentially improve the tumoral calcinosis resulting from mineral disorders associated with SHPT. We herein present the case of a 62-year-old male who had received 12 years of HD therapy, who was hospitalized for painful calcified masses around the left shoulder and bilateral iliac crests. He had undergone a total parathyroidectomy with forearm auto-transplantation for SHPT 5 years before hospitalization. However, his SHPT relapsed, and intravenous maxacalcitol therapy (15 mg/week) with calcium carbonate (3 g/day) had been administered for the last 4 years; the serum Ca and P levels remained above the upper limit recommended by the guidelines (10.7 serum Ca 12.8 mg/dL, 6.5 serum P 8.2 mg/dL) (2). On admission, the patient showed serum levels of corrected Ca of 12.6 mg/dL, P of 6.8 mg/dL, intact PTH of 320 pg/mL, and bone specific alkaline phosphatase of 34 U/L. He had been receiving HD during 4-h sessions three times per week with 3.0 mmol/L of Ca dialysate. Tc methoxy-isobutylisonitrile scintigraphy and neck ultrasonography disclosed two hyperactive parathyroid glands; one in the forearm and the other in the neck. Radiology disclosed a calcified mass around the left shoulder and bilateral iliac crests (Fig. 1). We concluded that the calcified masses were uremic tumoral calcinosis induced by persistent hypercalcemia and hyperphosphatemia, which could be attributed to the recurrent SHPT and inappropriate use of vitamin D and a Ca-based P binder. We discontinued the administration of maxacalcitol and calcium carbonate, and started treating him with sevelamer hydrochloride (3 g/day) and alphacalcidol (0.25 mg/day). A dose of 25 mg/day of cinacalcet hydrochloride was also started for the recurrent SHPT. At one month after adopting the new treatment, the serum Ca, P, and intact PTH levels were 9.2 mg/dL, 5.8 mg/dL, and 84.5 pg/mL, respectively, and these parameters remained within the recommended ranges thereafter (8.9 serum Ca 9.9 mg/dL, 4.3 serum P 5.8 mg/dL, 76.5 intact PTH 145.8 pg/mL). At