AI Article Synopsis

  • - Reports indicate that IgA nephropathy (IgAN), a kidney disease, can worsen or appear after starting TNF-α inhibitor (TNFi) therapy, particularly for Crohn's disease (CD), with unclear causes.
  • - Three patients developed kidney issues 2 to 6 years after beginning TNFi treatment, with biopsies confirming IgAN in two cases and IgAN with acute tubulointerstitial nephritis in one.
  • - All patients improved with additional corticosteroids and tonsillectomy while continuing TNFi therapy, highlighting a potential link between TNFi therapy for CD and increased risk of IgAN flare-ups.

Article Abstract

In recent years, increasing numbers of reports have described new onset or active disease flare of IgA nephropathy (IgAN) during administration of TNF-α inhibitor (TNFi) therapy for chronic inflammatory diseases. Crohn's disease (CD) is the most common indication for TNFi therapy in this clinical setting, but the underlying etiology of IgAN in such patients remains unclear. We report our experience with three patients who developed acute worsening of preexisting urinalysis abnormalities and kidney dysfunction approximately 2 to 6 years after TNFi administration for CD. Kidney biopsies at the time of kidney disease flare revealed IgAN in two patients and IgAN complicated by acute tubulointerstitial nephritis in one patient. The CD and IgAN in all three patients were successfully managed with additional corticosteroid therapy and tonsillectomy without discontinuing TNFi therapy. The clinical course of our patients and similar patients described in the literature suggests that TNFi therapy for CD is associated with a relatively high risk for new onset or disease flare of IgAN. This report discusses the possible involvement of Th1/Th2 imbalance on the immunological background of CD or IgAN.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294508PMC
http://dx.doi.org/10.1007/s13730-023-00836-0DOI Listing

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