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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.
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 ...
Glomerulonephritis (GN) is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, [ 1 ] but not all diseases necessarily have an inflammatory component.
Clinical features may include constitutional symptoms like fever, arthralgia, myalgia, loss of appetite, weight loss and fatigue.A variety of organs can be affected, which causes a wide range of symptoms such as cough, shortness of breath, hemoptysis (coughing up of blood), symptoms of kidney failure, skin manifestations (palpable purpura and livedo racemosa [1]), seizures or peripheral ...
In 2014 a study was completed to diagnose glomerulonephritis based on etiology. Using immunofluorescence and light microscopy, the investigators were determining the classification for the disease based on if the disease was immune complex mediated, pauci- immune, or complement mediated.
IgM nephropathy or immunoglobulin M nephropathy (IgMN) is a kind of idiopathic glomerulonephritis that is marked by IgM diffuse deposits in the glomerular mesangium. [1] IgM nephropathy was initially documented in 1978 by two separate teams of researchers.
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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]