How is pathogenesis of membranoproliferative glomerulonephritis?

➢ Type I MPGN may be caused by deposition of circulating immune complexes or by in situ immune complex formation with a planted antigen. ➢ The inciting antigen is not known. ➢ LM : glomeruli are large, have an accentuated lobular appearance, and show proliferation of mesangial and endothelial cells as well as infiltrating leukocytes ➢The GBM is thickened, and the glomerular capillary wall often shows a double contour, or “tram track,” appearance, especially evident with use of silver or periodic acid–Schiff (PAS) stains. ➢This “splitting” of the GBM is due to extension of processes of mesangial and inflammatory cells into the peripheral capillary loops and deposition of mesangial matrix as well as subepithelial immune complexes ➢The characteristic light microscopic glomerular manifestations are often referred to as membranoproliferative pattern of glomerular injury. ➢By electron microscopy, type I MPGN is characterized by discrete subendothelial deposits. ➢By immunofluorescence microscopy, C3 is deposited in an irregular granular pattern, and IgG and early complement components (C1q and C4) also often are present, indicative of an immune complex pathogenesis