Kemény E, Fillit M H, Mahabir R, Zabriskie B J
Morphol Igazsagugyi Orv Sz. 1989 Oct;29(4):287-91.
Authors studied the dispersion of immunoreactive HSPG with monoclonal antibody specific to protein nucleus of HSPG in renal diseases associated with nephrosis syndrome. Their results showed that the dispersion of HSPG in GBM does not fully agree with dispersion of anion linkage places known in literature. In membrane and diffuse proliferative lupus glomerulonephritis immunoreactive HSPG cannot be demonstrated in the place of immune deposits, concurrent with dispersion of anion places, while it appears in GBM newly developed round the deposits. Inconsistent with this, in glomerulonephritis having minimal changes, the anion loss of GBM is not associated with absence of nuclear protein, the immunoreactive HSPG remains intact. These observations reflected in literature indicate that--similarly to proteinuria--presumably, deficiency of anion linkage places of GBM is caused by different pathomechanisms.
