Abstract: SA-PO857
Carfilzomib-Associated Thrombotic Microangiopathy with Kidney Infarction Treated with Eculizumab
Session Information
- Glomerular Diseases: From Inflammation to Fibrosis - III
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: From Inflammation to Fibrosis
Authors
- Pietrzyk, Kristen L., University of California Davis, Davis, California, United States
- Mowrey, John, University of California Davis, Davis, California, United States
- Beck, Natalie M., University of California Davis, Davis, California, United States
- Jen, Kuang-Yu, University of California Davis, Davis, California, United States
- Wiegley, Nasim, University of California Davis, Davis, California, United States
Introduction
Thrombotic microangiopathy (TMA) results from endothelial cell injury that can lead to kidney injury. Drug-induced TMA (DITMA) is a rare but serious adverse effect of certain medications, including carfilzomib, a proteasome inhibitor used for multiple myeloma (MM). Parenchymal kidney infarction is a rare and severe complication of TMA, which can lead to significant acute kidney injury (AKI). We report a case of kidney infarction with anuric AKI associated with carfilzomib use.
Case Description
A 66 yo White woman with refractory IgG lambda MM began carfilzomib-based therapy. Kidney function was stable until 6 months after starting carfilzomib, when she experienced rapid decline in urine output and AKI with a creatinine of 7.4 mg/dL (baseline 0.6 two weeks prior), with thrombocytopenia and anemia. Within 2 days she was anuric and required hemodialysis (HD). Labs showed low haptoglobin and high lactate dehydrogenase, suggesting microangiopathic hemolytic anemia. ADAMTS-13, C3, C4, E. coli Shiga-like toxins were normal. A kidney biopsy confirmed TMA with fibrin thrombi affecting glomeruli and arterioles, plus parenchymal kidney infarction. (Fig 1) Carfilzomib was discontinued. Despite a negative complement genetic panel, eculizumab was started for severe TMA. Kidney function slowly improved, and HD was discontinued after 3 months.
Discussion
DITMA can be a rare but life-threatening complication of anti-cancer therapies. Carfilzomib has been associated with TMA. Although the exact mechanism is not fully understood, it is thought that Carfilzomib causes endothelial injury leading to TMA. Management of carfilzomib- associated TMA with kidney infarction involves prompt discontinuation of the drug. In severe cases, anti-complement therapy can be considered. A high index of suspicion is needed when caring for patients on this agent, as prompt recognition and management are essential for optimal patient outcomes.