<b>Methods:</b> MMP2 and MMP9 expression was detected by immunohistochemistry in sections from renal biopsy specimens with class III, class IV and class V LN (total <i>n</i> = 31), crescentic immunoglobulin A nephropathy (<i>n</i> = 6), pauci-immune glomerulonephritis (<i>n</i> = 7), minimal change disease (<i>n</i> = 2), mesangiocapillary glomerulonephritis (<i>n</i> = 7), diabetic nephropathy (<i>n</i> = 12) and histologically normal controls (<i>n</i> = 8).
IgA nephropathy (IgAN) is a complex syndrome characterized by deposition of IgA and IgA containing immune complexes (ICs) composed of IgG and complement C3 proteins in the mesangial area of glomeruli.
IgA nephropathy (IgAN), a frequent cause of chronic kidney disease worldwide, is characterized by mesangial deposition of galactose-deficient IgA1-containing immune complexes.
Immunoglobulin A nephropathy (IgAN) is considered as mesangiopathy since it initiates in the mesangium; however, other glomerular components are involved and the glomerular capillary wall offers the first contact to circulating macromolecular IgA1.
Bcl-2 downregulation in progressive IgAN was associated with an increased Bax/Bcl-2 ratio in glomerular epithelial cells and correlated with the downregulation of high endogenous podocyte p27(kip1) and p57(kip2) expression.
IgA(1) aberrant O-glycosylation is one of the main pathogeneses of IgA nephropathy (IgAN), and the core I beta3-Gal-T-specific molecular chaperone (Cosmc) mRNA expression of IgAN patients was significantly decreased.