Abstract
Mediators of immune glomerular injury may be divided into primary and secondary. Primary mediators include antibody and T cells and secondary include complement, infiltrating inflammatory cells, such as neutrophils, monocytes/macrophages and platelets, coagulation system, resident glomerular cells including mesangial, endothelial and epithelial cells, reactive oxygen metabolites, eicosanoids, proteolytic enzymes and a host of cytokines. Following initiation of immune glomerular injury with primary mediators, which in most cases is antibody, a complex set of interactions involving some or all of the secondary mediators occurs in the glomerulus, ultimately leading to the clinical manifestations of glomerular injury. The precise sequence and the mechanisms of these interactions are not fully defined but are under intense study. The identity of the putative antigens and why and how an autoimmune response develops are also not fully known.
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