TY - JOUR
T1 - Histologic localization of terminal complement complexes in renal diseases. An immunohistochemical study
AU - Ootaka, T.
AU - Suzuki, M.
AU - Sudo, K.
AU - Sato, H.
AU - Seino, J.
AU - Saito, T.
AU - Yoshinaga, K.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1989
Y1 - 1989
N2 - Histologic localizations of terminal complement complexes (TCCs) were examined and compared with clinical findings in 154 patients with various renal diseases. Immunohistochemical demonstration of TCCs was carried out on ethanol-fixed paraffin-embedded renal biopsy specimens by indirect immunoperoxidase technique. In glomerular diseases that are thought to be immune-complex glomerulonephritis (IC-GN), such as IgA-nephropathy, membraneous nephropathy, and systemic lupus erythematosus (SLE), TCCs were demonstrated in a pattern similar to that of immunoglobulins and C3, indicating that TCCs were induced by immune complexes. The intensity of TCC deposition was correlated with the morphologic destruction of glomeruli or serum creatinine levels with IgA-nephropathy, with urine protein in membraneous nephropathy, and with serum C4 in SLE. TCC deposits without IC were also observed in tissue damages without disease specificity such as glomerular or vascular sclerosis and tubulointerstitial lesions. These findings suggested the existence of various roles of TCCs in renal injury, according to IC-mediated or non-IC-mediated mechanism acting in individual diseases.
AB - Histologic localizations of terminal complement complexes (TCCs) were examined and compared with clinical findings in 154 patients with various renal diseases. Immunohistochemical demonstration of TCCs was carried out on ethanol-fixed paraffin-embedded renal biopsy specimens by indirect immunoperoxidase technique. In glomerular diseases that are thought to be immune-complex glomerulonephritis (IC-GN), such as IgA-nephropathy, membraneous nephropathy, and systemic lupus erythematosus (SLE), TCCs were demonstrated in a pattern similar to that of immunoglobulins and C3, indicating that TCCs were induced by immune complexes. The intensity of TCC deposition was correlated with the morphologic destruction of glomeruli or serum creatinine levels with IgA-nephropathy, with urine protein in membraneous nephropathy, and with serum C4 in SLE. TCC deposits without IC were also observed in tissue damages without disease specificity such as glomerular or vascular sclerosis and tubulointerstitial lesions. These findings suggested the existence of various roles of TCCs in renal injury, according to IC-mediated or non-IC-mediated mechanism acting in individual diseases.
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U2 - 10.1093/ajcp/91.2.144
DO - 10.1093/ajcp/91.2.144
M3 - Article
C2 - 2644805
AN - SCOPUS:0024495061
VL - 91
SP - 144
EP - 151
JO - American Journal of Clinical Pathology
JF - American Journal of Clinical Pathology
SN - 0002-9173
IS - 2
ER -