Table 1.

Complement involvement in non-antibody renal disease.

Focal segmental glomerulosclerosis	AP	C3, filtered through endothelium and glomerular basement membrane, activates through the AP and signals on podocytes to release glial cell line-derived neurotrophic factor that mediates the recruitment of parietal epithelial cell (PEC) in the glomerulus. PEC proliferation leads to sclerotic lesions
Membranoproliferative/C3 glomerulonephritis	AP	Mutations in complement components/regulators or acquired antibodies targeting complement components lead to excessive activation of the AP in the fluid phase, with glomerular deposition of complement debris
Atypical hemolytic uremic syndrome	AP	Environmental triggers may precipitate complement activation in subjects with genetic predisposition including mutations of complement components
Chronic kidney injury and fibrosis	MBL	Intrarenal complement activation, especially of C3, activates the renin–angiotensin system and the epithelial-to-mesenchymal transition
	AP

AP, alternative pathway, MBL, mannose-binding lectin.