Distribution of glomerular basement membrane antigens in diseased human kidneys

M. S. Schiffer, A. F. Michael, Y. Kim, A. J. Fish

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

We have previously shown, using high resolution epifluorescence microscopy, that heterologous rabbit antihuman glomerular basement membrane (GBM) antibody (RAHGBM) stains the GBM of normal human kidney in a bilaminar distribution along the endothelial and epithelial aspects of the GBM. In contrast, Goodpasture (GP) antibody stains a single linear component along the inner aspect of the GBM. In the present study, alterations in the staining reactivity of these components appear consistently to correlate with the known morphologic changes in various glomerulopathies. In idiopathic nephrotic syndrome, no changes from normal were observed. In membranous glomerulopathy, the inner RAHGBM antigen was preserved, but the outer antigen showed an irregular beaded alteration adjacent to membranous GBM immune deposits. In diabetic glomerulopathy, striking increase in the inner RAHGBM component was evident with markedly increased separation from the outer RAHGBM line. In membranoproliferative glomerulonephritis (MPGN), loss of the inner component but preservation of the outer RAHGBM line was evident; however, in type IMPGN, GP antigen was preserved as a single linear component, but in type II MPGN, there was splitting of GP antigen by GBM-dense deposit material into a double linear array along the endothelial and epithelial aspects of the GBM. These observations serve to substantiate our earlier findings that antigenic and nonantigenic components of the GBM are partitioned in the glomerular capillary wall; their selective characteristic alteration in various glomerulopathies additionally supports this view.

Original languageEnglish (US)
Pages (from-to)234-240
Number of pages7
JournalLaboratory Investigation
Volume44
Issue number3
StatePublished - 1981

Fingerprint

Dive into the research topics of 'Distribution of glomerular basement membrane antigens in diseased human kidneys'. Together they form a unique fingerprint.

Cite this