Abstract: FR-PO0445
Etanercept-Associated ANCA Vasculitis Presenting as Pauci-Immune Glomerulonephritis and Severe AKI
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Rodriguez, Yoan Ernesto, UF Health Jacksonville, Jacksonville, Florida, United States
- Makadia, Bhaktidevi, UF Health Jacksonville, Jacksonville, Florida, United States
- Liu, Shiguang, UF Health Jacksonville, Jacksonville, Florida, United States
- Seth, Sukriti, HCA Florida Ocala Hospital, Ocala, Florida, United States
Introduction
Anti–tumor necrosis factor-alpha (TNF-α) inhibitors such as Etanercept are widely used for autoimmune diseases but may rarely induce paradoxical ANCA-associated vasculitis. Renal involvement is uncommon but may present as rapidly progressive pauci-immune glomerulonephritis.
Case Description
A 77-year-old woman with psoriasis and rheumatoid arthritis previously treated with Etanercept presented with 10 days of anorexia, nausea, and fatigue. Baseline creatinine of 0.6–0.9 mg/dL increased to 3.3 mg/dL on admission, peaking at 3.89 mg/dL. Urinalysis showed hematuria; ultrasound showed normal kidneys without obstruction. Serology revealed positive p-ANCA (1:160), negative c-ANCA, and negative hepatitis B/C and HIV. Kidney biopsy demonstrated pauci-immune glomerulonephritis with focal segmental fibrinoid necrosis and medullary angiitis (Figure 1).
Figure 1. Pauci-immune glomerulonephritis: (1A) fibrinoid necrosis [arrow]; (1B) medullary angiitis with neutrophils, hemorrhage [arrow] (H&E, ×100).
The patient was treated with intravenous methylprednisolone 500 mg daily for 3 days, followed by prednisone 80 mg daily. Creatinine improved to 1.85 mg/dL. She was discharged with nephrology follow-up, and rituximab was planned for outpatient induction.
Discussion
TNF-α inhibitor–associated ANCA vasculitis is rare but should be considered in patients with unexplained AKI and active urine sediment after biologic exposure. Isolated renal involvement may occur. Proposed mechanisms include immune complex formation, complement activation, and cytokine imbalance leading to loss of immune tolerance.
Early recognition, discontinuation of the offending agent, kidney biopsy, and prompt immunosuppression are critical to preserve renal function. While withdrawal alone may lead to improvement, severe cases often require corticosteroids and additional therapy. Temporal association, exclusion of active disease, and recovery after withdrawal support a drug-induced etiology.