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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
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Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Uremic tumoral calcinosis is an uncommon but clinically significant complication in patients with end-stage kidney disease. It is characterized by the deposition of large calcified masses in periarticular soft tissues, leading to pain, fractures, restricted mobility, and impaired quality of life. Previous reports have indicated that severe hyperphosphatemia and/or hypercalcemia play a central role in its pathogenesis and that correction of these abnormalities may induce regression. However, therapeutic strategies for patients without marked calcium-phosphate imbalance have rarely been described. Here, we present a case in which regression of uremic tumoral calcinosis was achieved with intravenous etelcalcetide therapy, despite the absence of severe hypercalcemia or hyperphosphatemia.
A 45-year-old man undergoing maintenance hemodialysis for 11 years developed progressive soft-tissue calcifications around multiple joints, which gradually increased in size and became symptomatic. He ultimately sustained a femoral fracture related to tumoral calcinosis and required surgical fixation. After surgery, he was referred to our department for further management. On admission, laboratory data showed corrected serum calcium of 10.3 mg/dL, phosphate of 4.9 mg/dL, and intact parathyroid hormone (PTH) of 109 pg/mL. At that time, he was receiving cinacalcet hydrochloride and lanthanum carbonate.
We considered his intact PTH level was potentially underestimated, because blood sampling had been performed several hours after cinacalcet administration. Consequently, cinacalcet was discontinued and switched to intravenous etelcalcetide hydrochloride. Eleven months after referral, laboratory tests showed corrected calcium of 9.8 mg/dL, phosphate of 5.1 mg/dL, and intact PTH of 86.7 pg/mL. Radiographic evaluation demonstrated marked regression of the soft-tissue calcifications compared with baseline images.
This case demonstrated that switching from oral cinacalcet to intravenous etelcalcetide resulted in regression of uremic tumoral calcinosis, even in the absence of severe hypercalcemia or hyperphosphatemia. To the best of our knowledge, there have been no previous reports describing regression of tumoral calcinosis following etelcalcetide therapy. The underlying mechanism remains unclear. Etelcalcetide has been reported to produce more sustained reductions in serum calcium and PTH levels than cinacalcet in hemodialysis patients, and this pharmacological property may contribute to the dissolution of calcified deposits. Our experience suggests that intravenous etelcalcetide therapy could represent a valuable therapeutic option for uremic tumoral calcinosis in selected patients, potentially expanding current management strategies beyond conventional approaches focused solely on calcium-phosphate control.
