T. Oda et al., GLOMERULAR PROLIFERATION CELL-KINETICS IN ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN), Journal of pathology, 183(3), 1997, pp. 359-368
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.