Abstract: SA-PO1281
Immune Checkpoint Inhibitor-Associated Fulminant Myocarditis Successfully Treated with Plasma Exchange Combined with High-Dose Glucocorticoids: A Case Report
Session Information
- Onconephrology: Epidemiological Trends, Risk Stratification, and Clinical Outcomes
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Kakeya, Yumi, Medical Research Institute Kitano Hospital, PIIF Tazuke-Kofukai, Osaka, Japan
- Tsukamoto, Tatsuo, Medical Research Institute Kitano Hospital, PIIF Tazuke-Kofukai, Osaka, Japan
- Ishimura, Takuya, Medical Research Institute Kitano Hospital, PIIF Tazuke-Kofukai, Osaka, Japan
- Endo, Tomomi, Medical Research Institute Kitano Hospital, PIIF Tazuke-Kofukai, Osaka, Japan
- Matsubara, Takeshi, Medical Research Institute Kitano Hospital, PIIF Tazuke-Kofukai, Osaka, Japan
Introduction
Immune checkpoint inhibitor (ICI)-associated myocarditis is a rare but highly fatal immune-related adverse event. We report a case of severe myocarditis that developed during pembrolizumab therapy and was successfully saved with plasma exchange (PLEX) in addition to high-dose glucocorticoid therapy.
Case Description
The patient was a woman in her 60s with cancer of unknown primary origin, suspected to be renal cell carcinoma, with multiple bone metastases. She had been treated with pembrolizumab (200 mg) and the tyrosine kinase inhibitor axitinib (10 mg/day) for approximately three months, along with bisphosphonate therapy every three weeks. Two weeks after the second dose of pembrolizumab, she developed shortness of breath, nausea, vomiting, and loss of appetite. Eighteen days after the third dose, she presented to our emergency department because of worsening symptoms. Initial evaluation revealed severe cardiac dysfunction (EF 63 to 10–15%) and renal dysfunction (s-Cre 0.69 to 1.68 mg/dL), leading to emergency hospitalization. She subsequently developed worsening cardiogenic shock requiring continuous kidney replacement therapy, intra-aortic balloon pump (IABP) support, and high-dose catecholamines. Cardiac troponin I was markedly elevated at 0.1965 ng/mL (reference value ≤0.0156 ng/mL). She was diagnosed with pembrolizumab-induced fulminant myocarditis after exclusion of caronary artery disease. High-dose glucocorticoid therapy was initiated, and PLEX using one plasma volume with 5% albumin replacement was performed for two consecutive days to facilitate pembrolizumab removal. From the third hospital day, myocardial contractility gradually improved, allowing tapering of catecholamines and dialysis support. She was successfully weaned from IABP support on hospital day 10, and EF recovered to 57% by hospital day 38. The patient did not develop rhabdomyolysis or myasthenia gravis, as previously reported. Although myocardial biopsy was attempted, insufficient tissue prevented definitive histological diagnosis.
Discussion
This case demonstrates that a multidisciplinary approach including PLEX may be effective for severe pembrolizumab-induced fulminant myocarditis. Rapid collaboration among nephrologists, cardiologists, and oncologists is essential for successful intensive management of this life-threatening condition.