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Activation of the lectin complement pathway in post‐streptococcal acute glomerulonephritis
Author(s) -
Hisano Satoshi,
Matsushita Misao,
Fujita Teizo,
Takeshita Morishige,
Iwasaki Hiroshi
Publication year - 2007
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2007.02107.x
Subject(s) - complement system , lectin pathway , lectin , complement (music) , pathology , glomerulonephritis , immunology , medicine , microbiology and biotechnology , alternative complement pathway , biology , antibody , kidney , biochemistry , complementation , gene , phenotype
The aim of the present study was to elucidate the correlation between complement pathways and clinicopathological findings in post‐streptococcal acute glomerulonephritis (PSAGN). Immunohistological staining was performed on renal specimens obtained from 18 patients with PSAGN and 20 controls, using antibodies against IgG, IgA, IgM, C1q, C3c, C4, fibrinogen, factor B, C4‐binding protein (C4‐bp), C5b‐9, CD59, mannose‐binding lectin (MBL) and MBL‐associated serine protease‐1 (MASP‐1). Controls showed no deposition of any antibody. In seven patients, glomerular deposits of C3c, C4, factor B, C4‐bp, C5b‐9, CD59, MBL and MASP‐1 were found. In the remaining 11 patients, glomerular deposits of neither C4 nor MBL/MASP‐1 were found, and glomerular deposits of C3c, factor B, C5b‐9 and CD59 were evident. C4‐bp was detected in seven of these 11 patients. Glomerular deposits of fibrinogen were detected in five of seven patients with MBL/MASP‐1 deposits and in only two of 11 patients without MBL/MASP‐1 deposits. Hematuria was prolonged in three of seven patients with MBL/MASP‐1 deposits through follow up, whereas urinalysis was normal in all patients without MBL/MASP‐1 deposits. However, the histological indicators were not different between the two groups. To the authors' knowledge this is the first report to show that complement activation through both the alternative and lectin pathways is evident in some patients with PSAGN. Complement activation is promoted in situ in the glomerulus.