These results suggest that CTGF from mesangial cell, not podocytes, may be required for the upregulation of MCP-1expression not only in anti-GBM nephritis but also in other types of glomerulonephritis, such as IgA nephropathy, because CTGF expression and accumulation of macrophages in the mesangial area are documented in these glomerular diseases [38]. Here, CCN2 is linked to glomerular disorder.