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Abstract: TH-PO106

Calciphylaxis in a Patient With Tumor Lysis Syndrome due to T-Cell Lymphoma

Session Information

  • AKI: Mechanisms - I
    November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Ali, Mahmoud, Saint Barnabas Hospital, Bronx, New York, United States
  • Navarro Torres, Mariela, Montefiore Medical Center, Bronx, New York, United States
  • Fisher, Molly, Montefiore Medical Center, Bronx, New York, United States

Calciphylaxis is characterized by skin ischemia and necrosis and is most often observed in end-stage kidney disease (ESKD) or transplant patients. Non-ESKD associated calciphylaxis is uncommon but has been reported in patients with primary hyperparathyroidism, alcoholic liver cirrhosis, connective tissue disease and malignancy. We report an unusual presentation of calciphylaxis in the context of severe acute kidney injury (AKI) with tumor lysis syndrome (TLS) from T- cell lymphoma.

Case Description

A 46-year-old man with history of colon cancer treated with right hemicolectomy and chemotherapy and untreated T- cell lymphoma presented with respiratory distress. Laboratory results revealed a serum creatinine of 21.8 mg/dL compared to a baseline of 1.1 mg/dL seven months prior, potassium of 6.5 mEq/L, bicarbonate of <10 mEq/L, phosphorus of 15mg/dL, calcium of 7.6 mg/dL, uric acid of 8.9 mg/dL, lactate dehydrogenase of 542 U/L and severe pancytopenia. Spontaneous TLS in the setting of untreated lymphoma was suspected as the cause of his AKI. He was admitted to the intensive care unit and underwent emergent hemodialysis. Two days after admission, he was found to have a firm and tender lesion on the right medial thigh described as an ecchymosis with surrounding ulceration. A CT was negative for necrotizing fasciitis and the skin lesion was treated as a soft tissue infection. However, the lesion progressed, developing eschar. A punch skin biopsy was performed which confirmed a diagnosis of calciphylaxis. Intact parathyroid hormone was 228 pg/mL. Treatment included sodium thiosulfate, phosphorus control and hemodialysis. He was initiated on chemotherapy for his lymphoma and unfortunately, remained dialysis dependent.


Malignancy is a known risk factor for calciphylaxis but to our knowledge, this is only the second reported case of calciphylaxis in the setting of TLS. We hypothesize that our patient’s late presentation of TLS with fulminant AKI and severe metabolic derangements led to vascular calcium chelation and deposition. This case highlights the importance of calcium and phosphorus control in patients with TLS and risk factors for calciphylaxis.