Rapid regression of uremic calcinosis

A 28-year-old man with end-stage kidney disease from posterior urethral valve undergoing peritoneal dialysis for 3.5 years, presented with pain and swelling of both shoulders. Computed tomography revealed numerous massive calcifications in the subcutaneous tissue around both shoulder joints (Figure 1a). Severe pain and limited mobility led to the need for high doses of opioids. Serum calcium concentration was 2.46 mmol/l, parathyroid hormone 139.4 pmol/l, and phosphate 2.94 mmol/l. Uremic tumoral calcinosis was diagnosed, and cinacalcet hydrochloride 30 mg daily was started; peritoneal dialysis was replaced by hemodialysis. Parathyroid ultrasound revealed a 6-mm adenoma for which parathyroidectomy was performed. Three months later, there was a remarkable reduction in calcification (Figure 1b), accompanied by pain relief and improvement in joint mobility. Plasma parathyroid hormone and calcium normalized rapidly to 11.38 pmol/l and 2.16 mmol/l, respectively. Tumoral calcinosis can be from genetic, traumatic, or metabolic causes. The most common metabolic cause of tumoral calcinosis is chronic uremia. Uremic tumoral calcinosis most frequently affects large joints, such as the elbows, shoulders, hips, and knees. Uremic tumoral calcinosis is rare and has been particularly associated, albeit rarely, in patients on peritoneal dialysis. Treatment strategies that have been tried include switching to a low-calcium hemodialysis treatment, parathyroidectomy, noncalcium phosphate binders, and sodium thiosulfate. MN received consulting fees from Amicus, Sanofi, Astellas, Takeda, PSI CRO, and Swixx Biopharma; honoraria for lectures and presentations from Amicus, Takeda, Sanofi, AstraZeneca, Swixx Biopharma, Fresenius Kabi, and Amgen; and support for attending meetings and travel from Amicus, Sanofi, and Roche. TH received honoraria for presentations from Sanofi. All the other authors declared no competing interests.