In this study, we aimed to investigate whether p38 MAPK activity is associated with renal tubulointerstitial fibrosis in both an animal kidney fibrosis model and human IgA nephropathy and whether the anti-fibrotic effect of p38 MAPK inhibition can be confirmed using immunohistochemical staining for phosphorylated p38 in kidney tissue. This evidence concerns the gene MAPK14 and IgA glomerulonephritis.