Nephrology pp 990-995 | Cite as

In Situ Immune Complex Nephritis

  • Arnold Vogt

Abstract

Until the beginning of the nineteen eighties it was generally believed that glomerulonephritis was a “soluble complex disease” [1–3], the exception being that induced by anti-GBM antibody. Glomerular injury was considered to be the result of antigen-antibody deposits, with inflammation-inducing properties, which had previously been formed within the circulation [4]. This way of looking at things—for a long time it almost had the status of a dogma—was eventually challenged by Couser and Salant [5], who pointed at observations in passive Heymann nephritis, where the disease is not the result of circulating immune complexes but arises from combinations of the anti FxlA antibody with particular surface structures of the glomerular epithelial cells [6,7]. The main target molecule has been identified as a glycoprotein of 330 kD, known as gp 330 [8].

Keywords

Permeability Arthritis Filtration Polypeptide Proteinuria 

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Copyright information

© Springer Japan 1991

Authors and Affiliations

  • Arnold Vogt
    • 1
  1. 1.Institute of Medical MicrobiologyFreiburgFederal Republic of Germany

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