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Glomerular proliferating cell kinetics in acute post‐streptococcal glomerulonephritis (APSGN)
Author(s) -
Oda Takashi,
Yoshizawa Nobuyuki,
Takeuchi Akihiko,
Nakabayashi Iwao,
Nishiyama Junichiro,
Ishida Aki,
Tazawa Keiji,
Murayama Masahiro,
Hotta Osamu,
Taguma Yoshio
Publication year - 1997
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199711)183:3<359::aid-path939>3.0.co;2-b
Subject(s) - proliferating cell nuclear antigen , glomerulonephritis , pathology , biology , renal glomerulus , cell growth , kidney , immunohistochemistry , medicine , endocrinology , genetics
To investigate the time sequence of glomerular cell proliferation in acute 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 technique with monoclonal antibodies against proliferating cell nuclear antigen (PCNA) and various cell surface markers. Few, if any, PCNA + cells were observed in normal glomeruli, but many cells were positive for PCNA in the acute phase of APSGN. Glomerular PCNA + cells were observed either within glomerular tufts, or lining Bowman's capsule (parietal epithelial cells); the number of positive cells tended to decrease exponentially as the disease duration increased ( r =−0·91, P <0·0001). PCNA + cells within glomerular tufts were further identified by double immunostaining. PCNA was not found in PMN or T cells, but a small proportion 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 disease continued the proportion of mesangial cells (α‐smooth muscle actin + ) increased to about half of the total PCNA + cells within the tuft. These data indicate that the hypercellular glomeruli in APSGN are due not only to immune cell infiltration, but also to resident glomerular cell proliferation, probably induced by locally produced growth factors. © 1997 John Wiley & Sons, Ltd.