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30-489: ASOT may stand for: Antistreptolysin O titre A State of Trance , a radio show hosted by Armin van Buuren A Sound of Thunder (disambiguation) "A series of tubes" , phrase coined originally as an analogy by then-U.S. Senator Ted Stevens to describe the Internet in the context of opposing network neutrality . Asot Michael , Antiguan politician Topics referred to by

60-419: A nephritic syndrome characterised by proteinuria , and visible blood in the urine . IgA nephropathy is classically described as a self-resolving form in young adults several days after a respiratory infection. It is characterised by deposits of IgA in the space between glomerular capillaries . Henoch–Schönlein purpura refers to a form of IgA nephropathy, typically affecting children, characterised by

90-597: A nephrotic syndrome , a nephritic syndrome , acute kidney injury , or chronic kidney disease . They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differ in different types. Primary causes are intrinsic to the kidney. Secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders ( SLE , vasculitis), or diabetes. Glomerulonephritis refers to an inflammation of

120-441: A clinical diagnosis. The aim is to convert it . It is done by serological methods like latex agglutination or slide agglutination. ELISA may be performed to detect the exact titre value. To detect the titre value, by a non-ELISA method, one has to perform the above agglutination using a serial dilution technique. These antibodies produced against the bacteria cross-react with human antigens (mainly collagen ) and hence attack

150-416: A mild nephritic syndrome of moderately increased blood pressure, gross haematuria, and smoky-brown urine. Circulating immune complexes that deposit in the glomeruli may lead to an inflammatory reaction. Diagnosis may be made on clinical findings or through antistreptolysin O antibodies found in the blood. A biopsy is seldom done, and the disease is likely to self-resolve in children in 1–4 weeks, with

180-517: A poorer prognosis if adults are affected or if the affected children are obese. Membranoproliferative GN (MPGN), also known as mesangiocapillary glomerulonephritis, is characterised by an increase in the number of cells in the glomerulus, and alterations in the glomerular basement membrane . These forms present with the nephritic syndrome , hypocomplementemia , and have a poor prognosis. Three subtypes have been proposed: Rapidly progressive glomerulonephritis , also known as crescentic GN ,

210-406: A rash of small bruises affecting the buttocks and lower legs, with abdominal pain. Post-infectious glomerulonephritis can occur after essentially any infection, but classically occurs after infection with the bacteria Streptococcus pyogenes . It typically occurs 1–4 weeks after a pharyngeal infection with this bacterium, and is likely to present with malaise, a slight fever , nausea and

240-438: Is > 200 units/mL, but normal ranges vary from laboratory to laboratory and by age. The false negatives rate is 20 to 30%. If a false negative is suspected, then an anti-DNase B titre should be sought. False positives can result from liver disease and tuberculosis . Glomerulonephritis Glomerulonephritis ( GN ) is a term used to refer to several kidney diseases (usually affecting both kidneys). Many of

270-453: Is characterised by a sclerosis of segments of some glomeruli. It is likely to present as a nephrotic syndrome. This form of glomerulonephritis may be associated with conditions such as HIV and heroin abuse, or inherited as Alport syndrome . The cause of about 20–30% of focal-segmental glomerulosclerosis is unknown. On microscopy, affected glomeruli may show an increase in hyalin , a pink and homogeneous material, fat cells , an increase in

300-426: Is characterised by a rapid, progressive deterioration in kidney function. People with rapidly progressive glomerulonephritis may present with a nephritic syndrome . In management, steroid therapy is sometimes used, although the prognosis remains poor. Three main subtypes are recognised: Histopathologically, the majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into

330-552: Is characterised by an increased number of cells in the glomerulus. These forms usually present with a triad of blood in the urine , decreased urine production , and hypertension , the nephritic syndrome . These forms usually progress to end-stage kidney failure (ESKF) over weeks to years (depending on type). 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

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360-471: Is different from Wikidata All article disambiguation pages All disambiguation pages Anti-streptolysin O#Antistreptolysin O titre Increased levels of ASO titre in the blood could cause damage to the heart and joints. In most cases, penicillin is used to treat patients with increased levels of ASO titre. When the body is infected with streptococci, it produces antibodies against

390-585: Is no normal value. The presence of these antibodies indicates an exposure to these bacteria. However, as many people are exposed to these bacteria and remain asymptomatic, the mere presence of ASO does not indicate disease. A titre has significance only if it is greatly elevated (> 200), but a rise in titre demonstrated in paired blood samples taken days apart is more informative for diagnosis. The antibody levels begin to rise after 1 to 3 weeks of strep infection, peaks in 3 to 5 weeks and falls back to insignificant levels in 6 months. Values need to be correlated with

420-437: Is the most common cause of the nephrotic syndrome in children. Although no changes may be visible by light microscopy, changes on electron microscopy within the glomeruli may show a fusion of the foot processes of the podocytes lining the basement membrane of the capillaries of glomerulus. It is typically managed with corticosteroids and does not progress to chronic kidney disease . Focal segmental glomerulosclerosis

450-459: Is usually mild and overall prognosis is excellent. Fibronectin glomerulopathy is a rare form of glomerulopathy characterised by enlarged glomeruli with deposits in the mesangium and subendothelial space. The deposits have been shown to be fibronectin. This condition is inherited in an autosomal dominant fashion. About 40% of cases are due to mutations in the fibronectin ( FN1 ) gene located on chromosome 2 (2q34). Proliferative glomerulonephritis

480-516: The cellular matrix of various organs, mainly the heart, joints, skin, brain, etc. Antistreptolysin O titre ( AS(L)O titer or AS(L)OT ) is a measure of the blood plasma levels of antistreptolysin O antibodies used in tests for the diagnosis of a streptococcal infection or indicate a past exposure to streptococci. The ASOT helps direct antimicrobial treatment and is used to assist in the diagnosis of scarlet fever, rheumatic fever, and post infectious glomerulonephritis . A positive test usually

510-410: The glomerulus , which is the unit involved in filtration in the kidney. This inflammation typically results in one or both of the nephrotic or nephritic syndromes . The nephrotic syndrome is characterised by the finding of edema in a person with increased protein in the urine and decreased protein in the blood , with increased fat in the blood . Inflammation that affects the cells surrounding

540-412: The blood. This results in edema, as the oncotic pressure in tissue remains the same. Although decreased intravascular oncotic (i.e. osmotic) pressure partially explains the patient's edema, more recent studies have shown that extensive sodium retention in the distal nephron (collecting duct) is the predominant cause of water retention and edema in the nephrotic syndrome. This is worsened by the secretion of

570-613: The decrease in perfusion of juxtaglomerular apparatus , which may result in hypertension. This is characterised by forms of glomerulonephritis in which the number of cells is not changed. These forms usually result in the nephrotic syndrome . Causes include: Minimal change disease is characterised as a cause of nephrotic syndrome without visible changes in the glomerulus on microscopy. Minimal change disease typically presents with edema , an increase in proteins passed from urine and decrease in blood protein levels, and an increase in circulating lipids (i.e., nephrotic syndrome ) and

600-405: The diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component. As it is not strictly a single disease, its presentation depends on the specific disease entity: it may present with isolated hematuria and/or proteinuria (blood or protein in the urine ); or as

630-419: The females. This condition, similarly, is called Familial Membranous Glomerulonephritis. There have only been about nine documented cases in the world. Thin basement membrane disease is an autosomal dominant inherited disease characterized by thin glomerular basement membranes on electron microscopy. It is a benign condition that causes persistent microscopic hematuria . This also may cause proteinuria which

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660-410: The glomerular cells. Immunofluorescence demonstrates diffuse granular uptake of IgG . The basement membrane may completely surround the granular deposits, forming a "spike and dome" pattern. Tubules also display the symptoms of a typical Type III hypersensitivity reaction, which causes the endothelial cells to proliferate, which can be seen under a light microscope with a PAS stain. Prognosis follows

690-418: The glomerulus, podocytes , increases the permeability to proteins , resulting in an increase in excreted proteins. When the amount of proteins excreted in the urine exceeds the liver's ability to compensate, fewer proteins are detected in the blood – in particular albumin , which makes up the majority of circulating proteins. With decreased proteins in the blood, there is a decrease in the oncotic pressure of

720-419: The hormone aldosterone by the adrenal gland, which is secreted in response to the decrease in circulating blood and causes sodium and water retention. Hyperlipidemia is thought to be a result of the increased activity of the liver. The nephritic syndrome is characterised by blood in the urine (especially Red blood cell casts with dysmorphic red blood cells) and a decrease in the amount of urine in

750-401: The lung and bowel, infections such as hepatitis B and malaria , drugs including penicillamine , and connective tissue diseases such as systemic lupus erythematosus . Individuals with cerebral shunts are at risk of developing shunt nephritis , which frequently produces MGN. Microscopically, MGN is characterized by a thickened glomerular basement membrane without a hyperproliferation of

780-447: The mesangial matrix and collagen. Treatment may involve corticosteroids , but up to half of people with focal segmental glomerulonephritis continue to have progressive deterioration of kidney function, ending in kidney failure. Membranous glomerulonephritis may cause either nephrotic or a nephritic picture. About two-thirds are associated with auto-antibodies to phospholipase A2 receptor, but other associations include cancers of

810-457: The presence of hypertension . In this syndrome, inflammatory damage to cells lining the glomerulus are thought to result in destruction of the epithelial barrier, leading to blood being found in the urine. At the same time, reactive changes, e.g. proliferation of mesangial cells, may result in a decrease in kidney blood flow, resulting in a decrease in the production of urine. The renin–angiotensin system may be subsequently activated, because of

840-455: The rule of thirds: one-third remain with MGN indefinitely, one-third remit, and one-third progress to end-stage kidney failure . 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. In extremely rare cases, the disease has been known to run in families, usually passed down through

870-405: The same term [REDACTED] This disambiguation page lists articles associated with the title ASOT . If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=ASOT&oldid=1256020465 " Category : Disambiguation pages Hidden categories: Short description

900-433: The various antigens that the streptococci produce. ASO is one such antibody. A raised or rising levels can indicate past or present infection. Historically it was one of the first bacterial markers used for diagnosis and follow up of rheumatic fever or scarlet fever . Its importance in this regard has not diminished. Since these antibodies are produced as a delayed antibody reaction to the above-mentioned bacteria, there

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