What does this research mean for the field?

Severe, treatment-refractory hyperphosphatemia in patients with end-stage renal disease can contribute to the formation of calcified amorphous tumors (CATs), suggesting that strict phosphate control may reduce the risk of their development. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To describe the presentation, diagnosis, and surgical management of a rare intracardiac calcified amorphous tumor in a patient on peritoneal dialysis with treatment-resistant hyperphosphatemia.

September 5, 2026Peritoneal Dialysis International

Calcified amorphous tumor in a patient receiving peritoneal dialysis with severe, treatment-refractory hyperphosphatemia

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Authors

PKParth Kumar JWJennifer P. Woo NKNeeraja Kambham

Discussion

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Overview

Case report reveals intracardiac calcified amorphous tumor formation in a peritoneal dialysis patient with severe hyperphosphatemia, highlighting the importance of strict phosphate control.

Key Points

To describe the presentation, diagnosis, and surgical management of a rare intracardiac calcified amorphous tumor in a patient on peritoneal dialysis with treatment-resistant hyperphosphatemia.
Clinical, imaging, and histopathologic assessment of a 47-year-old female on peritoneal dialysis presenting with unremitting hyperphosphatemia (>10 mg/dL) and leg pain.
Diagnostic evaluation using transthoracic echocardiography to assess for infectious embolic sources, followed by surgical mass excision and histopathologic confirmation.
Transthoracic echocardiography identified a mobile intracardiac mass causing mitral valve dysfunction during an embolic workup.
Histopathologic examination of the surgically excised tissue definitively confirmed the mass to be a non-neoplastic calcified amorphous tumor.
Severe hyperphosphatemia had persisted despite trials of multiple phosphate binders, including sevelamer, calcium acetate, and tenapanor, predisposing the patient to extensive soft-tissue calcification.

Cite This Study

Kumar et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4046b95aff0620eb514 https://doi.org/10.1177/08968608261479962

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September 5, 2026Peritoneal Dialysis International

Calcified amorphous tumor in a patient receiving peritoneal dialysis with severe, treatment-refractory hyperphosphatemia

View Full Paper

Ask AI

Bookmark

Authors

PKParth Kumar JWJennifer P. Woo NKNeeraja Kambham

Discussion

Member takes

Overview

Case report reveals intracardiac calcified amorphous tumor formation in a peritoneal dialysis patient with severe hyperphosphatemia, highlighting the importance of strict phosphate control.

Key Points

To describe the presentation, diagnosis, and surgical management of a rare intracardiac calcified amorphous tumor in a patient on peritoneal dialysis with treatment-resistant hyperphosphatemia.
Clinical, imaging, and histopathologic assessment of a 47-year-old female on peritoneal dialysis presenting with unremitting hyperphosphatemia (>10 mg/dL) and leg pain.
Diagnostic evaluation using transthoracic echocardiography to assess for infectious embolic sources, followed by surgical mass excision and histopathologic confirmation.
Transthoracic echocardiography identified a mobile intracardiac mass causing mitral valve dysfunction during an embolic workup.
Histopathologic examination of the surgically excised tissue definitively confirmed the mass to be a non-neoplastic calcified amorphous tumor.
Severe hyperphosphatemia had persisted despite trials of multiple phosphate binders, including sevelamer, calcium acetate, and tenapanor, predisposing the patient to extensive soft-tissue calcification.

Cite This Study

Kumar et al. (2026) studied this question.

synapsesocial.com/papers/6a9bd4046b95aff0620eb514 https://doi.org/10.1177/08968608261479962

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