These data suggest that CTGF from mesangial cells, not podocytes, may be required for the upregulation of Ccl2 expression not only in anti-GBM nephritis but also in other types of glomerulonephritis such as IgA nephropathy or crescentic glomerulonephritis, because CTGF expression and accumulation of macrophages in mesangial area are documented in these glomerular diseases. Here, CCL2 is linked to glomerular disorder.