Pseudotumoral calcinosis in a haemodialysis patient
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NEPHROLOGY IMAGE
Pseudotumoral calcinosis in a haemodialysis patient Denis Bontemps1 · Philippe Brunet1,2 · Mickaël Bobot1,2 Received: 6 July 2020 / Accepted: 5 August 2020 © Italian Society of Nephrology 2020
Keywords Haemodialysis · Parathyroid hormone · Calcium · Bone A 58 year-old male on haemodialysis for 18 months due to polycystic kidney disease developed severe secondary hyperparathyroidism [serum PTH level: 726 pg/mL at diagnosis (normal range 15.1–65.1 pg/mL)]. He displayed increased calcium-phosphate product with calcium and phosphate levels of 2.27 and 3.47 mmol/L, respectively. Treatment included amlodipine, furosemide, sevelamer, ramipril and polystyrene sulfonate; however compliance was poor. Joint swelling appeared on the left wrist and right toes that had gradually increased over the past 10 months (Fig. 1a). Inflammation and autoimmune tests were negative. X-rays showed extensive periarticular calcifications of the toes and wrists (Fig. 1b, c). MRI showed multilobulated cystic calcifications of the wrist (Fig. 1d), supporting the diagnosis of pseudotumoral calcinosis (PTC). Hyperparathyroidism treatment was intensified and cinacalcet, systemic sodium thiosulfate injections (25 g three times a week) were administered, and dialysis time was increased. A low-calcium diet was introduced and treatment compliance improved. No surgery was performed regarding the high risk of incomplete resection and recurrence [1]. Clinical course slowly improved and pseudotumor volume decreased after several months of intensified treatment. PTC frequency is estimated between 0.5 and 3% in haemodialysis patients [1]. The most often affected areas are the subcutaneous soft tissues around the joints, predominantly in the upper limbs (shoulders, elbows or metacarpals) and hips.
Pathophysiology remains unclear but risk factors including increased calcium-phosphate product, hyperparathyroidism, metabolic alkalosis or hypervitaminosis D are reported [2]. Currently, no consensus treatment exists for PTC. Therapeutic strategies to control calcium-phosphate product, such as phosphate binders, increased dialysis time, calcimimetics, parathyroidectomy, or renal transplantation are based on case reports. To reduce hyperparathyroidism, subtotal parathyroidectomy is the most commonly reported treatment [1, 2]. The efficacy of local or systemic injections of sodium thiosulfate has also been reported. Regression of calcifications is usually slow. Although PTC is currently a rare complication of chronic kidney disease thanks to the improvement of current care, it is important to acknowledge this disease when dealing with a patient’s joint pain or swelling and uncontrolled calcium–phosphate product. Diagnosis can be easily confirmed on X-rays. In conclusion, to prevent and remove pseudotumoral calcinosis, appropriate dialysis time and a low-calcium diet are needed, allowing for calcium-phosphate product control.
* Mickaël Bobot [email protected] 1
Centre de Néphrologie et Transplantation Rénale, CHU de la Conception, AP-H
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