Mediation of immune glomerular injury.
This paper reviews current concepts of glomerular immune injury of both inflammatory and noninflammatory types. In noninflammatory lesions induced by antibody alone or C5b-9, the glomerular epithelial cell appears to be the principal target of injury. Similar mechanisms are probably operative in human diseases such as minimal change nephrotic syndrome and membranous nephropathy. In inflammatory lesions, circulating effector cells including neutrophils, macrophages, platelets, and probably lymphocytes as well as resident glomerular mesangial cells may mediate tissue injury. Human equivalents of these inflammatory lesions include most diseases associated with mesangial and/or subendothelial immune deposits and/or mesangial cell proliferation. Neutrophil-mediated injury appears to be consequent to both proteinases and oxidants, particularly the myeloperoxidase-H2O2-halide system. Platelets may be critically involved in neutrophil mediated injury as well. Platelets also mediate mesangial cell proliferation, probably by a release of platelet growth factors and stimulation of mesangial cell platelet-derived growth factor and platelet-derived growth factor receptor expression. Immunologically induced mesangial cell proliferation is associated with increased production of nephritogenic proteinase in vivo.
Couser
W G
WG
Department of Medicine, University of Washington Medical Center, Seattle.
D000818:Animals; D000937:Antigen-Antibody Reactions; D015938:Complement Membrane Attack Complex; D005921:Glomerulonephritis / Q000209:etiology; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology; D007678:Kidney Glomerulus / Q000276:immunology* / Q000293:injuries; D007962:Leukocytes / Q000276:immunology
D015938:Complement Membrane Attack Complex