A 62-year-old man with a history of stage 5 chronic kidney disease, type 2 diabetes mellitus, gout, and hypertension presented to the emergency department after having run out of peritoneal dialysate solution. The man was visiting California from Mexico. He also reported right knee and right elbow pain. He reported having undergone regular peritoneal dialysis until presentation, and he had a history of taking high-dose oral calcium acetate as prescribed by his physician in Mexico.
Physical examination. On physical examination, the man was found to have firm, fixed, nontender nodules on the right elbow and bilateral metacarpal joints. Pain was elicited in the right elbow on passive range of motion. On admission, laboratory test findings were notable for hypercalcemia (12 mg/dL) and hyperphosphatemia (7.4 mg/dL). Parathyroid hormone and vitamin D levels were normal. A radiograph of his right elbow revealed multilobular periarticular calcinosis (Figure 1). A computed tomography scan of the right elbow revealed multiple lobular structures with sedimentation, but without associated osseous erosion or destruction (Figure 2).
Diagnosis. Given the laboratory and radiographic findings, a diagnosis of secondary tumoral calcinosis was made.
Discussion. Tumoral calcinosis is a rare but benign condition involving calcium deposition, usually in the soft tissues around larger joints. Although tumoral calcinosis is considered benign, patients with it may experience discomfort and functional limitations at the sites of involvement.
The strict definition of tumoral calcinosis requires a hereditary predisposition to the disease and normal calcium levels.1 However, sporadic or idiopathic occurrences of tumoral calcinosis have been reported involving metabolic abnormalities.2 Secondary tumoral calcinosis has been associated with chronic kidney disease, usually with concomitant hyperparathyroidism, although this is not always present,3 as our patient’s case shows. Although our patient did have chronic kidney disease, his case was unique in that he did not have hyperparathyroidism, but rather appears to have developed the condition secondary to calcium acetate ingestion.
In general, treatment for tumoral calcinosis usually is symptom management; with normalization of phosphate and calcium levels, deposits can decrease in size. In rare cases, calcium deposits are surgically excised.3
Outcome of the case. After being admitted to the hospital, the patient was restarted on peritoneal dialysis, and his oral calcium acetate was discontinued. His calcium levels normalized during his hospital stay, and he was discharged with outpatient follow-up.
- Eisenberg B, Tzamaloukas AH, Hartshorne MF, Listrom MB, Arrington ER, Sherrard DJ. Periarticular tumoral calcinosis and hypercalcemia in a hemodialysis patient without hyperparathyroidism: a case report. J Nucl Med. 1990;31(6):1099-1103.
- Lykoudis EG, Seretis K, Ristanis S. Huge recurrent tumoral calcinosis needing extensive excision and reconstruction: report of a rare case and brief literature review. Aesthetic Plast Surg. 2012;36(5):1194-1197.
- Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. Radiographics. 2006;26(3):871-885.