Kidney Week

Abstract: TH-PO705

Unusual Suspect: Apixaban as a Cause of ANCA-Associated Vasculitis

Session Information

• Glomerular Diseases: Case Reports - 1
  October 24, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Perkit, Navya Reddy, Saint Vincent Hospital, Worcester, Massachusetts, United States

Navya Reddy Perkit, MD

• Suresh, Mithil Gowda, Saint Vincent Hospital, Worcester, Massachusetts, United States

Mithil Gowda Suresh, MD

• Singh, Jassimran, Saint Vincent Hospital, Worcester, Massachusetts, United States

Jassimran Singh, MD

• Vijayaprakash, Aviraag, Saint Vincent Hospital, Worcester, Massachusetts, United States

Aviraag Vijayaprakash, MD

• Rennke, Helmut G., Brigham and Women's Hospital, Boston, Massachusetts, United States

Helmut G. Rennke, MD

• Martin, Suzanne Gwen, Saint Vincent Hospital, Worcester, Massachusetts, United States

Suzanne Gwen Martin, MD, FASN

Introduction

Antineutrophilic cytoplasmic antibody (ANCA) vasculitis is a common cause of acute glomerulonephritis in adults, with drug-induced ANCA vasculitis (DIAV) being relatively rare.

Case Description

An 85-year-old female with stage IV chronic kidney disease (CKD), on apixaban for atrial fibrillation, presented with fatigue, weakness, and dyspnea. Exam showed clear lungs and new trace bilateral pitting pedal edema. She had proteinuria, hematuria, and creatinine of 5.41 mg/dL, up from baseline 2.5 mg/dL. Urine protein-creatinine ratio was elevated at 4.5 g/gCr. Renal biopsy indicated chronic-active focal proliferative, necrotizing, and crescentic glomerulonephritis with immune deposits. Serologies showed a high anti-MPO titer of 1:1997, with other autoantibodies negative. Given the elevated anti-MPO titer and biopsy findings, drug-induced ANCA vasculitis was considered. The patient was not on known causative medications. The temporal relationship with apixaban led to its discontinuation and transition to warfain. She received steroids along with two biweekly doses of rituximab which reduced the anti-MPO titer to 1:32 and proteinuria improved to 3 g/gCr.

Discussion

DIAV is a diagnosis of exclusion suggested by high anti-MPO titers, as seen in this case. The rapid improvement after discontinuation of apixaban and two doses of rituximab suggest her ANCA vasculitis was likely due to an offending agent, rather than spontaneous ANCA disease. Apixaban-induced ANCA vasculitis has not been previously reported, though apixaban-induced cutaneous leukocytoclastic vasculitis and drug-induced lupus suggest its potential for autoimmune phenomena. Prompt identification and treatment, including drug discontinuation and immunosuppressive therapy, are crucial for managing DIAV and preventing disease progression. Increased awareness and further research into apixaban-induced DIAV are essential due to its expanding use in CKD patients.