Complement activation in nonsystemic glomerular diseases in children.
All forms of glomerulonephritis (GN) in man seem to be immunologically mediated and the complement system appears as one of the most important mediators of renal injury. The study of complement activation is therefore of great help in the identification of the immunopathogenic process involved in the various types of glomerular diseases. After a review of the molecular events of complement activation and the methods used to study the complement system in man, we will attempt to summarize current knowledge concerning complement in nonsystemic glomerular diseases frequently encountered in children. The terms used are those descriptive of glomerular morphology as defined either by light microscopy and electron microscopy (endocapillary-proliferative GN with humps, extramembranous GN, membranoproliferative GN) or by immunofluorescent microscopy (mesangial IgA GN).
D001485:Basement Membrane / Q000473:pathology; D002648:Child; D002908:Chronic Disease; D003167:Complement Activation; D003176:Complement C3 / Q000378:metabolism; D003169:Complement Inactivator Proteins / Q000276:immunology; D003170:Complement Pathway, Alternative; D003171:Complement Pathway, Classical; D003165:Complement System Proteins / Q000032:analysis / Q000276:immunology; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis; D007668:Kidney / Q000473:pathology
D003176:Complement C3; D003169:Complement Inactivator Proteins; D007070:Immunoglobulin A; D003165:Complement System Proteins