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Related Experiment Videos

Bucillamine induces membranous glomerulonephritis.

Kiyotaka Nagahama1, Hiroshi Matsushita, Mitsuru Hara

  • 1Department of Pathology, Yokohama City University School of Medicine, Kanagawa, Japan. nag_k@med.yokohama-cu.ac.jp

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
|March 29, 2002
PubMed
Summary

Bucillamine (BCL) treatment in rheumatoid arthritis (RA) patients can cause membranous glomerulonephritis (MGN). This study reveals distinct immunoglobulin deposition patterns in BCL-induced MGN, suggesting a different pathogenesis than idiopathic MGN.

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Area of Science:

  • Nephrology
  • Rheumatology
  • Immunopathology

Background:

  • Rheumatoid arthritis (RA) is linked to various kidney diseases, including membranous glomerulonephritis (MGN).
  • Bucillamine (BCL), a drug for RA, shares similarities with d-penicillamine, known to induce MGN.
  • Previous reports on BCL-induced MGN lack detailed immunoglobulin analysis, hindering understanding of its pathogenesis.

Purpose of the Study:

  • To investigate the immunoglobulin deposition patterns in kidney biopsy specimens from RA patients treated with BCL who developed proteinuria.
  • To elucidate the pathogenesis of BCL-induced MGN by comparing it with idiopathic MGN.

Main Methods:

  • Analysis of seven kidney biopsy specimens from six RA patients treated with BCL.
  • Light microscopy to evaluate glomerular histopathology, including mesangial proliferation and capillary wall changes.

Related Experiment Videos

  • Immunofluorescence and electron microscopy to assess immunoglobulin (IgG subclasses) deposition and subepithelial deposits.

    • Main Results:

    • All specimens showed granular immunoglobulin G (IgG) deposition along glomerular capillary walls.
    • Five specimens exhibited deposition of IgG2 and/or IgG3 components, alongside IgG4.
    • BCL-induced MGN demonstrated different IgG subclass deposition and patterns compared to idiopathic MGN, with IgG3 potentially activating the classical complement pathway more efficiently.

    Conclusions:

    • Bucillamine-induced membranous glomerulonephritis in RA patients exhibits distinct immunoglobulin deposition characteristics.
    • The pathogenesis of BCL-induced MGN differs from idiopathic MGN, potentially involving more efficient activation of the classical complement pathway due to IgG3 deposition.