Urinary miR-29b, miR-29c and miR-93 levels correlated with the clinical disease severity of IgA nephropathy and with the down-stream signaling of transforming growth factor-beta (TGF-β) pathway [13], indicating that they may play important roles in the pathogenesis of renal fibrosis. This evidence concerns the gene TGFB1 and IgA glomerulonephritis.