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Pathogenicity of Human Anti-PLA 2 R1 Antibodies in Minipigs: A Pilot Study.

Linda Reinhard1, Thorsten Wiech2, Aline Reitmeier3

  • 1III. Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Journal of the American Society of Nephrology : JASN
|February 3, 2023
PubMed
Summary

Human anti-phospholipase A 2 receptor 1 (PLA 2 R1) antibodies cause membranous nephropathy (MN). This study in minipigs demonstrated that these antibodies induce MN characteristics, confirming their pathogenicity in this autoimmune kidney disease.

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Area of Science:

  • Nephrology
  • Immunology
  • Autoimmune Diseases

Background:

  • Primary membranous nephropathy (MN) is an autoimmune kidney disease with immune complex deposition in glomeruli, posing a risk for end-stage kidney disease.
  • Circulating anti-phospholipase A 2 receptor 1 (PLA 2 R1) antibodies are present in 70-80% of MN patients, correlating with prognosis, but direct evidence of pathogenicity was lacking.

Purpose of the Study:

  • To demonstrate the pathogenicity of human anti-PLA 2 R1 antibodies in inducing membranous nephropathy.
  • To utilize minipigs as a model for MN due to their intrinsic PLA 2 R1 expression on podocytes.

Main Methods:

  • Passive transfer of human anti-PLA 2 R1 antibody-containing plasma or purified IgG from MN patients to minipigs.
  • Monitoring of anti-PLA 2 R1 antibodies and proteinuria via Western blot, ELISA, and Coomassie staining.
  • Analysis of kidney tissues using immunohistochemistry, immunofluorescence, and electron microscopy.

Main Results:

  • Human anti-PLA 2 R1 antibodies bound to minipig PLA 2 R1 in vitro and in vivo.
  • Passive transfer induced histological features of early-stage MN, complement activation, and low-level proteinuria in minipigs.
  • Development of an autologous, later phase of disease was observed.

Conclusions:

  • Human anti-PLA 2 R1 antibodies are pathogenic in membranous nephropathy.
  • The minipig model successfully demonstrated the causal role of these antibodies in MN development.
  • Low-level proteinuria was observed in the heterologous phase of the disease.