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English: What is IgA nephropathy? IgA nephropathy, sometimes called Berger disease, is a type of nephritic syndrome where abnormal IgA antibody is formed, which results in immune complex deposition in the glomerular mesangium, leading to kidney disease. This video covers the pathophysiology, signs and symptoms, and treatment of IgA nephropathy.
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.
The symptoms at onset are very similar to IgA nephropathy and include abdominal pain, hematuria, edema, and oliguria. [ 18 ] Henoch–Schönlein purpura (HSP) - Often considered a systemic form of IgA nephropathy , Henoch–Schönlein purpura (HSP) is a systemic small-vessel vasculitis that is characterized by deposition of IgA antibody immune ...
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 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 ...
Treatment of secondary membranous nephropathy is guided by the treatment of the original disease. For treatment of idiopathic membranous nephropathy, the treatment options include immunosuppressive drugs and non-specific anti-proteinuric measures such as ACE inhibitors or angiotensin II receptor blockers.
Focal segmental glomerulosclerosis (FSGS) is a histopathologic finding of scarring of glomeruli and damage to renal podocytes. [2] [3] This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss. [3]
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