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Uraemic tumoral calcinosis in a peritoneal dialysis patient

A 37-year-old woman receiving peritoneal dialysis (PD) for 28 months developed progressive swelling and pain involving the bilateral shoulders, left elbow and right wrist. She was diagnosed with end-stage renal disease (ESRD) secondary to chronic glomerulonephritis. She had shown persistent hyperphosphataemia, hypercalcaemia and significant secondary hyperparathyroidism (SHPT) since the commencement of PD. A lowcalcium diet and low-calcium peritoneal dialysate (1.25 mmol/L) were given to control her hypercalcaemia. The PD schedule comprised four exchanges of 2 L of dialysate every day. A low-phosphate diet and noncalcium-containing phosphate binders (lanthanum carbonate 0.75 g 3 times daily with meals) was added to control her hyperphosphataemia. Also, active vitamin D was administered intermittently to control severe SHPT; however, serum calcium, phosphate and intact parathyroid hormone (iPTH) levels remained consistently high, and active vitamin D therapy was discontinued 3 months later. The corrected serum calcium level remained between 2.4 and 2.7 mmol/L (reference range, 2.0–2.9 mmol/L); the serum phosphate level ranged between 1.3 and 2.3 mmol/L (reference range, 0.7–1.6 mmol/L); the calcium-phosphorus product was between 3.4 and 5.9 mmol/L; and the iPTH level was between 61.8 and 134.3 pmol/L (reference range, 1.3–9.3 pmol/L). Cinacalcet was not administered in this patient, because it was not approved by the Chinese Food and Drug Administration until June 2014. The 24-h urine output was 0.25 L, with total (peritoneal and kidney) Kt/V of 1.953, and peritoneal transport status of high-average transport. At the time of admission for surgery, clinical examination demonstrated a solid tumour mass involving the bilateral shoulders, left elbow, and right wrist regions. Laboratory data were as following: serum creatinine, 724.9 μmol/L (reference range, 44.0–144.0 μmol/L); serum urea nitrogen, 21.6 mmol/L (reference range, 1.7–8.3 mmol/L); serum phosphorus, 2.1 mmol/L; iPTH, 113.3 pmol/L; serum alkaline phosphatase, 176.0 u/L (reference range, 35.0–100.0 u/L), and serum albumin of 18.1 g/L (reference range, 35.0–55.0 g/L). The level of the corrected serum calcium was normal at 2.4 mmol/L. Echocardiography showed the left ventricular ejection fraction (LVEF) of 52%. Plain radiographs showed large calcified masses involving the bilateral shoulders (diameter = 15.2 cm), left elbow (diameter = 8.5 cm), and right wrist region (diameter = 4.8 cm; Fig. 1A,D,F). An ultrasound and Tc–sestamibi scan showed four enlarged nodules approximately 2.0 cm in diameter without ectopic parathyroid tissue. Calcifications of coronary artery, abdominal aortic or valvular were not detected in this patient. After total parathyroidectomy (tPTX) + autotransplantation (AT), the patient developed apparent hungry bone syndrome and the iPTH level declined to 1.3 pmol/L, manifesting as rapid symptomatic hypocalcaemia (corrected serum calcium declined to 2.0 mmol/L) and normalisation of hyperphosphataemia (serum phosphorus declined to 1.5 mmol/L). During the follow up of 18 months, the corrected serum calcium concentration remained between 1.8 and 2.4 mmol/L; the serum phosphate concentration was between 1.1 and 1.6 mmol/L; the calcium-phosphorus product was between 2.2 and 5.4 mmol/L; and the iPTH level was between 1.3 and 10.6 pmol/L. Notably, uraemic tumoral calcinosis (UTC) was resolved dramatically within 3 months after the operation, and was diminished within 18 months. The left ventricular systolic function, as indicated by the LVEF, was dramatically improved from 52% to 62%. The patient declined radiograph to the left elbow and right wrist because she felt complete remission of symptoms. UTC is a rare manifestation of extraskeletal metastatic calcifications characterised by large masses containing calcium salt deposits, occurring most commonly in patients with ESRD. UTC is more common in women than men. The incidence of UTC in PD patients has been estimated to be 1.6%, and 0.5%–3% in haemodialysis (HD) patients. The striking involvement of the bilateral shoulders, left elbow, and right wrist in our case was rare. Most of the experience in managing UTC has been reported for patients on HD, with rare reports on PD. Although the pathogenesis of UTC is poorly understood, several factors appear to increase risk, such as female gender, hypercalcaemia, hyperphosphataemia, increased calcium-phosphate product, hyperparathyroidism, a high level of fibroblast growth factor 23, the use of calciumcontaining phosphate binders and active vitamin D. Risk factors in this patient included uncontrolled SHPT, hypercalcaemia, hyperphosphataemia, and the use of active vitamin D for controlling SHPT. Most risk factors are derived from individual case reports or from small retrospective studies, but not confirmed in epidemiologic studies. A review of the English literature yielded 26 cases of UTC in patients undergoing PD. In this limited sample, 17 of 26 patients were female. Nearly all patients had hyperphosphataemia and an elevated calcium-phosphate product, regardless of serum calcium and iPTH levels. The primary focus of therapy should be to optimise calcium and phosphate homeostasis. Thus, aggressive control of hyperphosphataemia with non-calcium-containing