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Kidney Week

Abstract: TH-PO700

Infliximab-Induced Secondary IgA Nephropathy in a Patient with Rheumatoid Arthritis

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Gajjar, Prachi, Trumbull Regional Medical Center, Warren, Ohio, United States
  • Parmar, Parth, Trumbull Regional Medical Center, Warren, Ohio, United States
  • Gajjar, Hetvi, Pramukhswami Medical College, Karamsad, Gujarat, India
  • Shrestha, Sepiya, Trumbull Regional Medical Center, Warren, Ohio, United States
  • Shah, Dhruvil K., Trumbull Regional Medical Center, Warren, Ohio, United States
  • Magnani, Kashish, Surat Municipal Institute of Medical Education and Research, Surat, Gujarat, India
Introduction

IgA Nephropathy is the most common primary glomerular disease in the world, characterized by the antibody formation against Galactose-deficient IgA1, which gets deposited in the glomerulus. It can be primary or secondary. Secondary causes associated are liver disease, celiac disease, HIV infection and medications like anti-tumour Necrosis Factor α therapy.

Case Description

A 69-year-old male with polyarticular erosive rheumatoid arthritis, atrial fibrillation, hypertension, chronic kidney disease stage 3a with baseline creatinine of 1.5 mg/dL came with a complaint of fatigue and dark urine for a month. His rheumatoid arthritis was well controlled with Infliximab infusions eight weekly for last 10 years. On admission, he had acute kidney injury with five fold rise in creatinine without oliguria. Urinalysis showed microscopic hematuria and moderate proteinuria. Renal biopsy suggested IgA Nephropathy with mesangial proliferation with IgA deposits. Infliximab was stopped, and the patient was given a tapering dose of steroids. After around two months of stable renal function with steroids, rheumatologist resumed Infliximab, which resulted in a similar episode of acute kidney injury, which was again resolved by stopping the medicine. This made it more evident that Infliximab was the culprit behind secondary IgA nephropathy.

Discussion

There have been case reports on Infliximab and other TNFα inhibitors causing secondary IgA Nephropathy. The overall aetiology of medication-induced IgA Nephropathy, along with the underlying autoimmune conditions, is not well understood. One hypothesis suggests antibodies against the glycan structure of TNFα inhibitors lead to interaction with the presence of aberrant IgA1 molecules in the serum, forming large polymeric IgA complexes. More molecular-level studies are needed to get more robust evidence of such an association.

Mesangial Proliferation on PAS stain