Nephrology Dialysis Transplantation, Vol 13, Issue 3 608-616, Copyright © 1998 by Oxford University Press
J Soma, T Saito, T Ootaka, H Sato and K Abe
Background: An important aspect in glomerular
nephritic processes is the enhanced influx of leukocytes into the
glomerulus. Methods: To investigate the mechanisms of
intraglomerular leukocyte infiltration in IgA nephropathy (IgA-N) and
membranoproliferative glomerulonephritis type I (MPGN-I), we
immunohistochemically examined the intraglomerular expression of leukocyte
function-associated antigen-1 (LFA-1, CD11a/CD18), macrophage-1 (Mac-1,
CD11b/CD18) and intercellular adhesion molecule-1 (ICAM-1, CD54) together
with glomerular deposition of C3c and fibrinogen.
Results: In IgA-N (n=42),
LFA-1+ cells were distributed mainly in glomeruli
with intense expression of ICAM-1, and there was a positive correlation
(P<0.001) between the number of LFA-1+ cells
and the degree of ICAM-1 expression. Mac-1+ cells
had no correlation with glomerular C3c deposition, but had a significant
correlation with fibrinogen deposition (P<0.05). The number of
LFA-1+ cells was significantly greater than of
Mac-1+ cells (P<0.05). The number of
LFA-1+ cells was strongly correlated with that of
CD68+ cells (P<0.00001). In MPGN-I (n=43), on
the contrary, Mac-1+ cells correlated only with C3c
deposition (P<0.001), and they were observed mainly in peripheral
loops of glomerular capillaries where C3c was deposited with a similar
distribution. However, there was no relationship between
LFA-1+ cells and ICAM-1 expression. The number of
Mac-1+ cells was greater than that of
LFA-1+ cells (P<0.0001), and most
Mac-1+ cells were identical to
CD15+ cells. Conclusion: These
results indicate the possibility that different mechanisms may cause
glomerular leukocyte infiltration in various forms of human
glomerulonephritis. The LFA-1/ICCAM-1 pathway may play an important role in
glomerular leukocyte infiltration in IgA-N, while the Mac-1/complement
pathway may be important in MPGN-I. The former may promote mainly the
infiltration of CD68+ cells, and the latter may
promote that of CD15+ cells. In addition,
Mac-1+ cells may act as fibrinogen and complement
receptors in IgA-N and MPGN-I, respectively. Key
words: adhesion molecules; complements; glomerular leukocytes
infiltration; IgA nephropathy; membranoproliferative glomerulonephritis
ORIGINAL ARTICLES
Differences in glomerular leukocyte infiltration between IgA nephropathy and membranoproliferative glomerulonephritis
The Second Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-77, Japan; Corresponding author
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