MCP-1 can stimulate related cells to promote the release of superoxide anions and lysosomal enzymes, resulting in direct damage to the kidney; it can also activate and promote monocytes to secrete TGF-β and other factors that can cause cell fibrosis, thereby promoting glomerular sclerosis, causing fibrosis of the renal interstitium, and ultimately the progression of IgA nephropathy to end-stage renal failure [24, 25]. This evidence concerns the gene CCL2 and IgA glomerulonephritis.