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Abstract: TH-PO152

Bevacizumab-Associated Thrombotic Microangiopathy Treated with Eculizumab

Session Information

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Hilburg, Rachel, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Palmer, Matthew, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Burger, Robert, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Chiang, Elaine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Graul, Ashley, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Patankar, Sonali, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Geara, Abdallah Sassine, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Hogan, Jonathan J., University of Pennsylvania, Philadelphia, Pennsylvania, United States
Introduction

Bevacizumab is a recombinant monoclonal antibody neutralizing VEGF-A that has demonstrated efficacy as an anti-neoplastic agent. Thrombotic microangiopathy (TMA) is a well-described complication of VEGF inhibitors. A previous case series described treatment of VEGF inhibitor-associated TMA with eculizumab. Here, we present two cases of bevacizumab-associated TMA with biopsy-proven kidney involvement who were treated with eculizumab.

Case Description

Case 1: A 68 yo woman with recurrent, metastatic ovarian high-grade serous carcinoma received pegylated liposomal doxorubicin (PLD) and bevacizumab. She developed new onset HTN, proteinuria (UPCR 0.6 from 0.1 g/g), and AKI (SCr 1.5 from 0.9 mg/dL). Her HTN and AKI improved with holding bevacizumab. Bevacizumab was restarted and she again developed HTN, proteinuria (UPCR 3.1 g/g) and AKI (SCr 1.5 mg/dL). Despite drug discontinuation for over two months, she developed hypertensive emergency, PRES, nephrotic syndrome, and microangiopathic hemolytic anemia (haptoglobin <30 mg/dL, LDH 282 U/L, schistocytosis) consistent with systemic TMA. A kidney biopsy showed severe chronic TMA. Eculizumab was initiated (900mg IV x 4 doses). Hemolysis and HTN resolved, and SCr improved to 2.7 mg/dL.

Case 2: A 52 yo woman with HTN and stage IIIC poorly differentiated serous carcinoma was treated for progression of disease with PLD, atezolizumab, and bevacizumab. She had near complete response but developed palmar-plantar erythrodysesthesia attributed to PLD followed by worsening HTN, proteinuria (UPCR 1.6 from 0.1 g/g), and AKI (SCr 1.7 from 0.7 mg/dL). Bevacizumab was held, but SCr increased to 2.2 mg/dL. Further evaluation revealed evidence of systemic TMA (haptoglobin <30 mg/dL, LDH 425 U/L, schistocytosis). Kidney biopsy showed chronic TMA. Despite several months off bevacizumab, her TMA failed to improve. She received eculizumab, which was stopped after 2 doses for rash of unclear etiology. However, her hemolysis resolved, thrombocytopenia improved, and SCr stabilized at 1.6 mg/dL.

Discussion

We present two cases of severe bevacizumab-associated TMA with renal involvement who had evidence of disease improvement or stabilization with eculizumab treatment. The role of complement in VEGF inhibitor-associated TMA and treatment with complement blockade deserves further study.