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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.
IgA nephropathy, also known as Berger's disease, is the most common type of glomerulonephritis, and generally presents with isolated visible or occult hematuria, occasionally combined with low grade proteinuria, and rarely causes a nephritic syndrome characterised by proteinuria, and visible blood in the urine. IgA nephropathy is classically ...
IgA nephropathy is the most common glomerulonephritis worldwide; the global incidence is 2.5/100,000 per year amongst adults. [1] Aggressive Berger's disease is on the NORD list of rare diseases. [2] Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus.
IgA nephropathy (Note: Contrast time of onset with Post-streptococcal Glomerulonephritis) - Most commonly diagnosed in children who recently had an upper respiratory tract infection (URI). Symptoms typically present within 1–2 days of a non-specific URI with severe flank / abdominal pain, gross hematuria (characterized by dark brown or red ...
[1] IgA nephropathy is the most common cause of MesPGN. [3] It is thought abnormally glycosylated IgA form polymers and deposit in the mesangium. [3] Subsequently, IgA immune complexes bind to IgA receptors on mesangial cells and induce injury to mesangial cells through release of cytokines and growth factors that promote infiltration of ...
Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney.It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). [4]
MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults. [3] It should not be confused with membranous glomerulonephritis, a condition in which the basement membrane is thickened, but the mesangium is not.
The changes are indistinguishable from those observed in IgA nephropathy. [12] Microphotograph of a histological section of human skin prepared for direct immunofluorescence using an anti-IgA antibody, the skin is a biopsy of a patient with Henoch–Schönlein purpura. IgA deposits are found in the walls of small superficial capillaries (yellow ...