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Once Shiga toxin enters the circulation it can travel throughout the body and cause the wide array of end organ damage and the multitude of symptoms seen with HUS. Shiga toxin gains entry to cells by binding to globotriaosylceramide (Gb3) which is a globoside found on cell membranes, it is found throughout the body including the surface of the ...
Membranoproliferative glomerulonephritis (MPGN) - Another type of glomerulonephritis that is caused primarily by immune complex deposition in the glomerular mesangium and glomerular basement membrane thickening, which activates the complement cascade and damages the glomerulus. This damage leads to inflammation in the glomerulus and can present ...
Thin basement membrane disease must be differentiated from the other two common causes of glomerular hematuria, IgA nephropathy and Alport syndrome. The history and presentation are helpful in this regard: [citation needed] In Alport syndrome, there is often a family history of kidney failure, which may be associated with hearing impairment.
Glomerulonephrosis is a non-inflammatory disease of the kidney presenting primarily in the glomerulus (a glomerulopathy) as nephrotic syndrome.The nephron is the functional unit of the kidney and it contains the glomerulus, which acts as a filter for blood to retain proteins and blood lipids.
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, [2] activating the complement system and damaging the glomeruli. MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults. [3]
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.
Diabetic glomerulonephritis in a person with nephrotic syndrome. Secondary causes of nephrotic syndrome have the same histologic patterns as the primary causes, though they may exhibit some differences suggesting a secondary cause, such as inclusion bodies. [24] They are usually described by the underlying cause, such as: [citation needed]
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.
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