GLOMERULAR PROLIFERATION CELL-KINETICS IN ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN)

To investigate the time sequence of glomerular cell proliferation in a cute human glomerulonephritis, renal biopsy tissues were examined from 15 acute post-streptococcal glomerulonephritis (APSGN) patients (who were biopsied 1-31 days after onset), using an immunoperoxidase techni que with monoclonal antibodies against proliferating cell nuclear anti gen (PCNA) and various cell surface markers. Few, if any, PCNA(+) cell s were observed in normal glomeruli, but many cells were positive for PCNA in the acute phase of APSGN. Glomerular PCNA(+) cells were observ ed either within glomerular tufts, or lining Bowman's capsule (parieta l epithelial cells); the number of positive cells tended to decrease e xponentially as the disease duration increased (r=-0.91, P<0.0001). PC NA(+) cells within glomerular tufts were further identified by double immunostaining. PCNA was not found in PMN or T cells, but a small prop ortion of macrophages were PCNA(+) Most of the remaining PCNA(+) cells were resident glomerular cells; the proportion of PCNA(+) endothelial cells (CD31(+)) was over 80 per cent in the early phase, but as the d isease continued the proportion of mesangial cells (a-smooth muscle ac tin(+)) increased to about half of the total PCNA(+) cells within the tuft, These data indicate that the hypercellular glomeruli in APSGN ar e due not only to immune cell infiltration, but also to resident glome rular cell proliferation, probably induced by locally produced growth factors. (C) 1997 John Wiley & Sons, Ltd.