Characterised histologically by alterations in the GBM and mesangium and by proliferation of glomerular cells
Type I MPGN characterised by electron dense subendotheliaal deposits occurs in association with hepatitis B and C antigenemia, SLE, infected atrioventricular shunts, and extra-renal infections
The pathogenesis of type II MPGN, also known as dense-deposit disease, appears to be excessive complement activation
proliferation of mesangial and endothelial cells as well as infiltrating leukocytes. The GBM is thickened, and the glomerular capillary wall shows a double contour, or "tram track," appearance
2 types of MPGN have different ultrastructural and immunofluorescence microscopic features
Membranoproliferative glomerulonephritis, showing mesangial cell proliferation, increased mesangial matrix (staining black with silver stain), basement membrane thickening and focal splitting, accentuation of lobular architecture, swelling of cells lining peripheral capillaries, and influx of leukocytes.
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