FIG. 535.6 Cellular location of injury during glomerulonephritis. Mesangial cells are directly exposed to the circulation. Deposition of immune complexes within these cells is typically seen in disorders such as immunoglobulin A (IgA) nephropathy; it results in proliferation and expansion of the cells, leading to hematuria, proteinuria, and renal impairment. Epithelial cells, in conjunction with basement membrane, allow filtration of plasma solutes but retard passage of cells and plasma proteins. Disease related to these cells is typified by the presence of subepithelial deposits and flattening of the foot processes that engage the basement membrane, resulting in disruption of the filtration barrier and proteinuria. Endothelial cell disease can result from deposition of immune complex (as occurs in mesangiocapillary glomerulonephritis), attachment of antibody to the basement membrane (Goodpasture disease), or trauma and activation of coagulation (hemolytic-uremic syndrome). Endothelial cell proliferation and necrosis are accompanied by leukocyte accumulation, and rupture of the basement membrane, crescent formation, and disruption of glomerular architecture can develop. A nephritic or rapidly progressive presentation ensues.
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