Abstract: TH-PO0550
Under the Shadow of Stones: Adalimumab-Induced IgA Vasculitis with Renal Involvement
Session Information
- Glomerular Diseases: IgAN, IgA Vasculitis, and More
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Usama, Zainab, Ochsner Health, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States
- Alshwayat, Anas Radi Issa, Ochsner Health, New Orleans, Louisiana, United States
Introduction
Tumor necrosis factor-α inhibitors are widely used for inflammatory bowel disease but can rarely cause paradoxical immune-mediated complications, including vasculitis. IgA vasculitis related to anti-TNF therapy is uncommon, and renal involvement may be missed when alternative causes of acute kidney injury are present.
Case Description
A 64-year-old man with Crohn disease on long-term adalimumab, recurrent nephrolithiasis, hypertension, heart failure with reduced ejection fraction, and Chronic Kidney Disease stage 3b with baseline creatinine 1.9 mg/dL was referred for acute kidney injury initially attributed to obstructive nephrolithiasis. He underwent stone removal and ureteral stent placement. During nephrology evaluation, urine microscopy revealed dysmorphic erythrocytes, acanthocytes, and red blood cell casts, suggesting a glomerular rather than isolated urologic source of hematuria. He also had worsening proteinuria and marked hematuria. Shortly after his next adalimumab injection, he developed a palpable purpuric rash. Skin biopsy confirmed IgA vasculitis. Kidney biopsy was deferred because of high procedural risk. Serologic evaluation was unrevealing except for ANA positivity. Given worsening kidney function with creatinine 3.2 mg/dL, urine protein-creatinine ratio 1.7 g/g, hematuria >100 RBC/hpf, biopsy-proven IgA skin vasculitis, and temporal association with adalimumab, adalimumab was discontinued and corticosteroids were started. Four weeks later, creatinine improved to 2.1 mg/dL, urine protein-creatinine ratio decreased from 1.7g/g to 0.65 g/g, hematuria improved to 14 RBCs/HPF, and active urinary sediment resolved.
Discussion
This case highlights adalimumab-induced IgA vasculitis with renal involvement in the setting of a competing urologic diagnosis. Urinary sediment microscopy identified acanthocytes and red blood cell casts before purpura, redirecting the evaluation toward glomerular disease. The clinical course and improvement after drug withdrawal and corticosteroids support a drug-induced process. This case emphasizes the value of urinary sediment microscopy and the need to consider anti-TNF–associated vasculitis when glomerular hematuria and purpura develop during biologic therapy.