Nephrology Dialysis Transplantation, Vol 14, Issue 4 881-886, Copyright © 1999 by Oxford University Press
K Lhotta, R Wurzner and P Konig
Background. Mannose-binding lectin (MBL), a member of
the collectin family, binds to various oligosaccharides and activates the
classical pathway of complement independent from Clq. At present it is
unknown whether this so-called lectin pathway of complement activation
plays a role in the pathogenesis of human glomerulonephritis.
Methods. Direct immunofluorescence of 84 renal
biopsies using an MBL-specific monoclonal antibody and antibodies directed
against IgG, IgA, IgM, Clq, C3, and terminal complement complex (TCC) was
performed. Serum MBL levels of 50 patients were determined by enzyme-linked
immunosorbent assay. Results. MBL was detected in the
glomeruli of patients with lupus nephropathy (15 of 16), membranous
nephropathy (10/15), membranoproliferative glomerulonephritis type I (5/6)
and anti-GBM nephritis (2/4). MBL deposition paralleled that of
immunoglobulins, Clq, C3, and TCC but was less intense as compared to Clq.
Focal segmental deposits of MBL were present in focal segmental
glomerulosclerosis (4/6), IgA nephropathy (3/11), amyloidosis AL (1/4), and
advanced renal fibrosis (2/2). Here MBL staining was identical to IgM and
C3 and considered an unspecific entrapment of MBL in sclerotic lesions in
these cases. No significant difference in MBL serum levels was observed
between normal controls and patients with lupus nephritis, membranous
nephropathy, membranoproliferative glomerulonephritis, focal segmental
sclerosis, minimal change disease or IgA nephropathy. In patients suffering
from membranous nephropathy with (n=10) or without
(n=5) glomerular MBL deposits serum creatinine, C3,
C4, serum protein, and proteinuria were not statistically different.
Conclusion. MBL is present in the glomeruli of
patients with glomerulonephritis involving deposition of IgG and activation
of the classical pathway of complement. We propose that MBL binds to
agalactosyl oligosaccharides of IgG that terminate in
N-acetylglucosamine. The extent to which the lectin
pathway of complement contributes to overall complement activation in the
glomeruli remains unknown, but is likely to be marginal.
Keywords: complement; glomerulonephritis; lupus
nephropathy; mannose-binding lectin; membranous nephropathy
ORIGINAL ARTICLES
Glomerular deposition of mannose-binding lectin in human glomerulonephritis
Department of Internal Medicine, Innsbruck University Hospital and Institute for Hygiene, University of Innsbruck, Innsbruck, Austria; Corresponding author address: Nephrologisches Labor, Medizinische Universitatsklinik, Anichstrasse 35, A-6020 Innsbruck, Austria
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