Kidney Week

Abstract: TH-PO0518

Adalimumab-Associated IgAN in a Patient with Recurrent Scleritis

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

• Olivera-Latorre, Samille A., University of South Florida, Tampa, Florida, United States

Samille A. Olivera-Latorre, MD, MPH

• Tiwari, Ani, University of South Florida, Tampa, Florida, United States

Ani Tiwari, MBBS

• Ahmed, Amir, University of South Florida, Tampa, Florida, United States

Amir Ahmed, MBBS

• Miyahara, Fernanda Yumi, University of South Florida, Tampa, Florida, United States

Fernanda Yumi Miyahara, MD

• P Narayanankutty, Naveen, University of South Florida, Tampa, Florida, United States

Naveen P Narayanankutty, MD, FASN

Introduction

TNF-α inhibitors are widely used for inflammatory diseases but may cause paradoxical immune-mediated complications. IgA nephropathy during TNF-α inhibitor therapy is rare and underrecognized, particularly in adults.

Case Description

44-year-old woman with a 15-year history of recurrent scleritis treated with adalimumab after prior immunosuppression who developed hematuria, proteinuria, and renal dysfunction (creatinine rose from 0.7–0.8 to 1.5 mg/dL). Urinalysis showed dysmorphic RBC and significant proteinuria (24-hr urine protein 2.19 g/day; UPCR 3.5 g/g). Workup for secondary causes was negative; complements were normal. Imaging unremarkable. Kidney biopsy showed mesangial and endocapillary hypercellularity, segmental sclerosis, mild interstitial fibrosis, and crescents (Oxford M1E1S1T1C1) with dominant mesangial IgA deposition. Adalimumab was discontinued, and corticosteroids with mycophenolate were initiated. Follow-up demonstrated improvement in creatinine (1.2 mg/dL) and proteinuria (UPCR 1.2 g/g).

Discussion

The case highlights an association between TNF-α inhibitor therapy and IgAN. The temporal relationship with drug exposure and improvement after discontinuation supports a drug-induced process. TNF-α blockade may promote immune dysregulation and aberrant IgA deposition. Clinicians should consider biologic-associated glomerular disease in patients with new hematuria or proteinuria. Early recognition and drug withdrawal may stabilize renal function and limit progression.