A quantitative immunohistochemical study of the expression of mesangial alpha-smooth muscle actin and the proliferation marker Ki-67 in glomerulonephritis in man.

Using a specific marker 1A4 (DAKO), a quantitative evaluation of alpha-smooth muscle actin (ASMA) in glomeruli has been performed on human renal biopsies from patients suffering from acute, postinfectious, endocapillary glomerulonephritis (GN; 9 biopsies), IgA nephropathy (11 biopsies) and membranoproliferative GN (11 biopsies) and appropriate controls expressing a very weak ASMA reactivity. A significantly increased expression was found in all categories of GN. The glomeruli from IgA nephropathy showed variation of ASMA expression (range 0.1-27.7%) and a pattern of ASMA staining that was mesangial, global and diffuse. This pattern was also seen in cases of IgA nephropathy with focal, segmental, proliferative GN. In all biopsies, the glomerular cell number and proliferation index was determined. All the categories of GN showed significantly increased glomerular cellularity and proliferation index. Among the three types of GN, the glomerular cellularity and proliferation was lowest in IgA nephropathy. The mean number of Ki-67-positive intraglomerular nuclei and the proliferation index were both significantly correlated with the mean number of glomerular cell nuclei. Morphometric estimates demonstrate increased ASMA expression in types of GN with different prognosis. This finding and the lack of correlation with proliferation markers together indicate that the role of ASMA in GN is complex. This method of ASMA estimation may be useful in further studies of its role in disease activity and prognosis.