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KMID : 0359919950140030268
Korean Journal of Nephrology
1995 Volume.14 No. 3 p.268 ~ p.276
an Ultrastructural Study on the Experimental IgA Nephropathy in Mice



Abstract
IgA nephropathy was induced in a group of ICR mice by oral administration of bovine gamma globulin (BGG) and polio vaccine to clarify the mechanism of immune complex deposits and hematuria morphologically.
The removed kidneys were investigated by light microscopy, immunofluorescent microscopy and electron microscopy.
By direct immunofluorescence, IgA was detected in 26 out of total 30(36.7%) in polio vaccine group. ultrastructurally, electron dense deposits were noted in mesangium, paramesangium, subendothelium and intramebranous region. Extracellular
destruction
was expressed as splitting, thinning, eventual rupture of the basement membrane and mesangiolvsis. It is assumed that this ruptured basement membrane may result in hematuria due to leakage of red blood cells. The ultrastructural changes of
endothelial
cells are edema, destruction of the fenestrated structure and detachment from themesangial region. Therefore it can be postulated that IgA immune complexes may enter directly into mesangial matrix from capillary lumina through these destructed
endothelial cells.
The ultrastructural alterations of glomerular anionic sites were studied using polyethyleneimine (PEI) Prominent common findings in the glomeruli were few PEI particles in electron dense deposits in the mesangial and subendothelial area and
marked
reduction in glomerular anionic sites covered with deposits. The absence of PEI perticle means loss of anionic sites. So it is suggested that the loss of PEI particle is closely related with change of permeability of capillary basement membrane
and
cause proteinuria.
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