| Nephritides |
Pathological findings |
Possible initial triggers of necrosis |
| Lupus Nephritis |
-Mesangial proliferation, crescent formation, glomerular necrosis |
-Complement activation |
| -ROS generation by infiltrating cells |
| -Granular mesangial orsubendothelial or subepithelial IgG deposits |
-Cytokine secretion |
| IgA Nephropathy |
-Glomerular hypercellularity (mesangial or endocapillary), acute tubular necrosis, and crescent formation |
-Cytokine secretion by mesangial cells |
| -Enhanced TGF-(3 release by mesangial cells leading to sclerosis |
-ROS generation by infiltrating cells. |
| -Linear IgA deposits |
-Complement activation |
| Anti-GBM nephritis |
-Wide spread glomerular crescents |
- Complement activation |
| -Glomerular fibrinoid necrosis |
| -Linear IgG deposits |
| Pauci immune glomerulonephritis |
- Crescents and fibrinoid necrosis often containing neutrophil granule constituents |
-ROS generated by neutrophil activation |
| -Cytokines and proteases released by neutrophils |
