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When these are subjected to immunofluorescence, three patterns can be observed: linear, granular and negative (pauci-immune). [1] The linear and granular patterns are examples of positive immunofluorescence that are associated as follows: Goodpasture syndrome (linear pattern), post-streptococcal glomerulonephritis (granular), and diffuse ...
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney function, [4] [5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months) [5] with glomerular crescent formation seen in at least 50% [5] or 75% [4] of glomeruli seen on kidney biopsies.
The neutrophils bind to p-ANCAs and subsequently release inflammatory cytokines, reactive oxygen species and lytic enzymes that cause endothelial injury resulting to inflammation and necrosis of the small vessels. [4] The damage that is caused in the kidneys is specifically called necrotizing and crescentic glomerulonephritis. [5]
As the glomerulonephritis progresses, the tubules of the kidney become infected, leading to atrophy and hyalinisation. The kidney appears to shrink. Treatment with corticosteroids is attempted if the disease progresses. [citation needed] In extremely rare cases, the disease has been known to run in families, usually passed down through the females.
Pathogenesis of post-streptococcal glomerulonephritis includes injury to the glomerulus by immune complexes (IgG) passively trapped in the glomerulus, which leads to an inflammatory response from recruited immune cells, cytokines, chemical mediators, and complement and coagulation cascade activation. [5]
IgA nephropathy (IgAN), also known as Berger's disease (/ b ɛər ˈ ʒ eɪ /) (and variations), or synpharyngitic glomerulonephritis, is a disease of the kidney (or nephropathy) and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney.
Over time, many of these immune complexes might find their way to the glomerulus, and they cause an activation of the classical complement pathway, leading to complement protein deposition right along side the immune complex deposits. The second way involves the inappropriate activation of the alternative pathway of complement.
Tumors, medications, allergic reactions, and infectious organisms are some of the recognized triggers for these conditions, even though the precise cause of many of them is unknown. Immune complex disease, anti-neutrophil cytoplasmic antibodies , anti-endothelial cell antibodies, and cell-mediated immunity are examples of pathogenetic factors.