Kidney Week

Abstract: TH-PO0532

Biologic Therapy and Renal Autoimmunity: A Case of Infliximab-Associated Crescentic IgAN in Crohn Disease

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

• Khan, Asmad, TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Asmad Khan, MD

• Salih, Noman, TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Noman Salih, MD

• Ullah, Izhar, TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Izhar Ullah, MD

• Ofori, Eric K., TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Eric K. Ofori, MD

• Arif, Ali, TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Ali Arif, MD, MBBS, FASN

• Hanif, Muhammad Owais, TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Muhammad Owais Hanif, MD

• Khan, Kazi S., TidalHealth Peninsula Regional, Salisbury, Maryland, United States

Kazi S. Khan, MD

Introduction

Tumor necrosis factor-alpha (TNF-α) inhibitors such as infliximab are cornerstone therapies in Crohn's disease but have been associated with paradoxical immune-mediated complications, including IgA nephropathy (IgAN). Infliximab-associated IgAN is rare and incompletely understood and distinguishing it from Crohn's disease–associated IgAN remains a diagnostic challenge.

Case Description

A 20Y/F with Crohn's disease on infliximab for 5 years presented with AKI (Cr 0.9 → 1.79 mg/dL), hematuria, and substantial proteinuria (UMaCR 1994 μg/mg). Serologies (C3, C4, MPO, PR3, anti-GBM) were negative. Kidney biopsy revealed IgA nephropathy with crescentic and sclerosing features (Oxford: M0E0S1T0C1) and granular mesangial IgA on immunofluorescence. Infliximab was discontinued for suspected drug-induced IgAN. The patient received pulse IV steroids followed by a high-dose oral prednisone taper, with subsequent normalization of Cr and marked improvement in proteinuria.

Discussion

Infliximab may paradoxically induce autoimmune disease through cytokine dysregulation and immune complex formation. Infliximab disrupts mucosal IgA homeostasis in gut-associated lymphoid tissue, promoting the generation of galactose-deficient IgA1, a pathogenic form that preferentially deposits in the glomerular mesangium, triggering mesangial injury.[1] In this case, improvement in renal function following drug discontinuation favors a drug-induced etiology rather than Crohn's disease–associated IgAN, although the 2 entities may coexist. The presence of crescentic lesions (C1) highlights a more aggressive phenotype with increased risk of progression, supporting the decision for prompt immunosuppressive therapy. [2]
Clinicians should maintain vigilance for renal involvement in patients receiving infliximab. This case underscores the importance of regular urinalysis and renal function monitoring during infliximab therapy to ensure timely diagnosis.