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Related Experiment Video

Updated: Jan 27, 2026

Author Spotlight: Investigating the Potential of Chinese Herbal Medicinal Active Dioscin in Treating IgA Nephropathy
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Adalimumab-induced IgA nephropathy.

Aneesha Kaur Bhagat Singh1,2, Andrew Sujeevan Jeyaruban3, Gregory John Wilson4

  • 1Internal Medicine, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.

BMJ Case Reports
|April 3, 2019
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor alpha (TNFα) inhibitors can cause Immunoglobulin A nephropathy (IgAN). This case shows IgAN resolved with infliximab after adalimumab withdrawal, remaining stable with infliximab therapy.

Keywords:
crohn’s diseasedrug interactionsdrugs: gastrointestinal systeminflammatory bowel diseaseunwanted effects/adverse reactions

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Area of Science:

  • Nephrology
  • Rheumatology
  • Gastroenterology

Background:

  • Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis.
  • Biological agents, particularly tumor necrosis factor alpha (TNFα) inhibitors, are increasingly recognized as potential causes of secondary IgAN.
  • Crohn's disease (CD) is a chronic inflammatory condition often treated with TNFα inhibitors.

Observation:

  • A 39-year-old woman with a history of Crohn's disease (CD) treated with adalimumab developed renal dysfunction and hematuria.
  • Renal biopsy confirmed IgA nephropathy (IgAN), leading to adalimumab cessation.
  • Following a CD flare, infliximab was initiated, leading to remission of both CD and IgAN.

Findings:

  • This case presents the first documented instance of IgAN developing as a complication of adalimumab, a TNFα inhibitor.
  • The IgAN remained in remission even after switching to a different TNFα inhibitor, infliximab.
  • Successful management of both CD and IgAN was achieved with infliximab.

Implications:

  • This case highlights the importance of considering TNFα inhibitors as a potential etiology for IgAN in patients with inflammatory diseases.
  • It suggests that switching to a different TNFα inhibitor may be a viable strategy for managing IgAN in this context.
  • Further research is warranted to understand the mechanisms underlying TNFα inhibitor-induced IgAN and to establish optimal treatment guidelines.