The aim of this study was to determine the relationship of α-smooth muscle actin (ASMA) and the proliferation marker Ki-67 of glomerulonephritis (GN). Immunohistochemical stainings with the usual streptavidin-biotin peroxidase method were performed on 86 renal biopsies using monoclonal 1A4 and Ki-67. The results of the quantitative evaluation of ASMA and Ki-67 were analyzed for the correlation between positive value of ASMA and Ki-67 in different GN. ASMA expressions of glomeruli were highest in acute post-infectious GN [APGN; 16.9 Fraction Volume (FV)%], followed by unclassified proliferative GN (UnGN; 12.5 FV%), membranoproliferative GN (MPGN; 8.5 FV%), lupus nephritis (LupusN; 6.3 FV%), IgA nephritis (IgAN; 5.6 FV%), and normal control (0.1 FV%). The Ki-67 staining was considerably elevated in lupusN (4.3 Ki-67 positives/glomerulus), APGN (2.7), MPGN (2.5), UnGN (1.66), IgAN (0.5), compared with that in normal control group (0.1 Ki-67 positives/glomerulus). Ki-67 value in each category of glomerular diseases was significantly different from that in the control biopsies (p<0.004). The relationship between morphometric results of ASMA and Ki-67 was statistically significant regardless of the diagnosis. (rs=0.425, p=0.000, ASMA= 0.1113+0.1665 Ki-67). In conclusion, the immunohistochemical assessment of ASMA and Ki-67 expression in GN might be a reliable indicator for the progression of GN. This study indicates that active cellular proliferation is associated with increased actin deposition in glomeruli.