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      Nephritogenic Glycoprotein

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          Proliferative glomerulonephritis was induced in rats by a single injection in the hind footpads of the glycoprotein isolated from pronase digests of homologous renal cortex, in spite of the evidence that the glycoprotein no longer possessed the antigenic activity with respect to producing the nephrotoxic antibody. In rats given the glycoprotein (without trichloroacetic acid (TCA) treatment) prepared from pronase digests of homologous renal cortex, morphologic changes of proliferative glomerulonephritis were followed (3–4 months after injection) by those of typical membranous glomerulonephritis with an immunofluorescent ‘granular’ pattern, but in animals which received the glycoprotein (with TCA treatment), the morphologic changes of the kidney were those of proliferative glomerulonephritis with an immunofluorescent ‘mesangiaΓ pattern throughout the whole course. Morphologic changes of membranous glomerulonephritis induced in the group given the glycoprotein (without TCA treatment) can be explained by an immune-complex mechanism, superimposed on the basic pathogenesis (common to both groups) of proliferative glomerulonephritis with immunofluorescent ‘mesangial’ pattern.

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          Author and article information

          S. Karger AG
          02 December 2008
          : 22
          : 4-6
          : 504-513
          3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, and Department of Pathology, School of Medicine, Keio University, Tokyo
          181519 Nephron 1978;22:504–513
          © 1978 S. Karger AG, Basel

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          Pages: 10
          Original Paper


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