The etiology plays a role in the specific mechanism of DPGN. Usually the deposition of immune-complexes (antigen-antibody complex) that activates the complement system are involved. The antibodies that form immune complexes deposits or they bind directly to the nonglomerular antibodies present. Immune-complexes are combinations of DNA, anti-dsDNA ubiquitin, and other proteins in DPGN that are associated with lupus nephritis. C1q, the first component of the complement system, encounters conformational change that leads to C3 convertase breaking C3 into C3a and C3b. C3a, C5a, IL-8 are all chemotactic factors of the activated complement system. Part of their role is to recruit polymorphonuclear cells and leukocytes. Interleukins like IL-6, tumor necrosis factor-alpha, and interferon-gamma, that cause cell injury, are released. Mesangial proliferation is caused by activated platelets. Another mechanism involves antibodies formed against alpha-3 chain of collagen IV. Their deposition occurs in the sub-epithelial spaces. This causes proteinuria by damaging the basement membrane and creating a loss of negative charge. These are anionic deposits that fail to cross the membrane. Cationic deposits that cross the membrane are then deposited into sub-epithelial spaces. Then the disease advances and crescents are formed. Crescents are a combination of epithelial cells, activated macrophages, and fibrin. They lead to rupturing of small blood vessels, ultimately causing necrosis and sclerosis. Basic Summary The glomeruli are the filters in the kidneys. When working normally they will move the waste, excess electrolytes, and unnecessary fluid from the bloodstream to the urine. When a person develops DPGN, over 50% of the glomeruli<unk>  become inflamed. There is also an increase in mesangial, epithelial, and endothelial (proliferative) cells. Inflammatory cells are also rapidly developed. This causes damage to the kidneys and does not allow for proper filtration.
Diffuse proliferative nephritis
Shunt nephritis
Focal proliferative nephritis
Lupus nephritis
Membranous glomerulonephritis
IgA nephropathy
Trench nephritis
Acute proliferative glomerulonephritis