Histologic localization of terminal complement complexes in renal diseases: an immunohistochemical study

• Published in: American journal of clinical pathology Vol. 91; no. 2; pp. 144 - 151
• Main Authors: OOTAKA, T, SUZUKI, M, SUDO, K, SATO, H, SEINO, J, SAITO, T, YOSHINAGA, K
• Format: Journal Article
• Language: English
• Published: Chicago, IL American Society of Clinical Pathologists 01.02.1989
• Subjects: Antibody Specificity; Biological and medical sciences; Complement Membrane Attack Complex; Complement System Proteins - immunology; Complement System Proteins - metabolism; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Immunohistochemistry; Kidney Diseases - immunology; Kidney Diseases - metabolism; Kidney Diseases - pathology; Kidney Glomerulus - metabolism; Kidney Glomerulus - pathology; Kidneys; Medical sciences; Nephrology. Urinary tract diseases; Urinary system involvement in other diseases. Miscellaneous; Human; Immunohistochemistry; Renal disease
• ISSN: 0002-9173; 1943-7722
• DOI: 10.1093/ajcp/91.2.144

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, membranous 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 in IgA-nephropathy, with urine protein in membranous 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.