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Abstract: PO2188

Immune Checkpoint Inhibitor-Induced p-ANCA Multiorgan Vasculitis

Session Information

  • Onco-Nephrology - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Montanez, Marelle, University of Texas Health Science Center at Houston, Houston, Texas, United States
  • Lin, Jamie, University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Mamlouk, Omar, University of Texas Health Science Center at Houston, Houston, Texas, United States
  • Abudayyeh, Ala, University of Texas MD Anderson Cancer Center, Houston, Texas, United States
  • Glass, William F., University of Texas Health Science Center at Houston, Houston, Texas, United States
Introduction

Use of immune checkpoint inhibitors (ICIs) has led to improved mortality in melanoma, lung cancer, and lymphoma. ICIs augment immunologic reaction against tumor cells via blockade of cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed cell death-protein 1 (PD-1), or programmed death-ligand 1 (PD-L1). Renal complications from ICI use are uncommon but can involve development of glomerular diseases and interstitial nephritis. Below we present a case of p-ANCA vasculitis in a patient on ICI therapy.

Case Description

A 52-year-old female with adenocarcinoma of the right lung (T2N2) s/p right lower lobectomy, cisplatin/vinorelbine, radiation therapy, and durvalumab was hospitalized for evaluation of new onset oral blisters, fevers, hemoptysis, skin lesions, and acute kidney injury. Her creatinine rose to 3.2 mg/dL (baseline of 0.5 mg/dL). Urinalysis revealed >180 RBCs and 17 WBCs per high power field with a urine protein to creatinine ratio (UPCR) of 2.63 g/g. ANCA titers were positive for PR-3 antibody of 4.6 units. Patient underwent renal biopsy, which revealed evidence of renal vasculitis involving all glomeruli and crescents in 4 out of 20 glomeruli. There was concern for endocarditis with vegetation seen on echocardiogram; however, with negative blood cultures the etiology was attributed to autoimmunity (vasculitis) rather than infection. The patient was aggressively treated for ANCA vasculitis with pulse steroids, plasmapheresis, and rituximab (1g given 2 weeks apart). She had a dramatic improvement in her skin lesions, hemoptysis, cardiac and renal function. Two months following her last rituximab infusion, she has not had further hematuria, her UPCR remains < 0.5 g/day, and creatinine is stable at 1.2 mg/dL. PET/CT continues to demonstrate clinical remission of her underlying cancer.

Discussion

With the dramatic cancer responses seen in patients receiving immune checkpoint therapy, there has also increased understanding associated toxicities. Although reports of ANCA positive vasculitis from ICI has been reported; this case is unique due to the multiorgan involvement of her vasculitis including the heart valves. Aggressive treatment with steroids, plasmapheresis, and rituximab has proven effective without hindering her tumor response.