Glomerulonephritis (GN) is a form of autoimmunity in which apoptosis may be a double-edged sword. Resolution of GN can be promoted by apoptosis of infiltrating leucocytes and excess resident glomerular cells, leading to efficient anti-inflammatory clearance by macrophages and mesangial cells. However, unscheduled apoptosis in glomerular cells, especially epithelial cells ('podocytes') may drive progression of GN to hypocellular, nonfunctional scar. Defects in clearance of apoptotic cells may also have deleterious local effects, in addition to promoting autoimmunity itself. Nevertheless, there is strong promise for novel therapies based on new knowledge of apoptosis in GN, especially in regulation of leucocyte clearance from the inflamed glomerulus.