Poststreptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia
Poststreptococcal glomerulonephritis is one of the oldest recognized renal .. in children: observed association with the T1 subtype of group A streptococcal. Poststreptococcal GN is a form of glomerulonephritis. It is caused by an infection with a type of streptococcus bacteria. The infection does not. specific nephritogenic strains of group A beta-hemolytic streptococcus. A correlation between renal functions, morphologic damage and.
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Developing PSGN after strep throat or scarlet fever is most common in young, school-age children. Developing PSGN after impetigo is most common in preschool-age children. Doctors can test urine samples to look for protein and blood. Doctors can also do a blood test to see how well the kidneys are working. They can also determine if a patient recently had a group A strep infection.
Poststreptococcal glomerulonephritis (GN)
Decreasing swelling edema by limiting salt and water intake or by prescribing a medication that increases the flow of urine diuretic Managing high blood pressure hypertension through blood pressure medication People with PSGN who may still have group A strep in their throat are often provided antibiotics, preferably penicillin. While rare, long-term kidney damage, including kidney failure, can occur.
It is likely that this localization is facilitated by the cationic charge of this antigen, as earlier studies have postulated Vogt, et al. Recent studies have demonstrated that the Fc portion of antibodies directed to SPEB bind to the C-terminal domain rSPEBand that immunization with this domain prevents group A streptococcal infection in mice Tsao, et al. Their studies showed that histones enter the circulation after streptococcal lysis and are capable of inducing in situ immune-complex formation.
Finally, recent evidence suggests that there is not a single nephritogenic antigen, since studies by Beres et al. Notably, in studies of the Str. The alternate pathway of complement activation is usually activated in APSGN and is manifested by a depression of C3 levels.
Poststreptococcal glomerulonephritis (PSGN)
However, some patients may also have a reduction in their levels of C1 and C4. In addition, in some patients, there may also be complement activation by the lectin pathway Ohsawa, et al. It has long been known that there is an overexpression of cellular adhesion molecules ICAM-1, LFA-1 and infiltration of lymphocyte and macrophages in the glomeruli of these patients.
This anti-IgG reactivity may be due to autoantigenic changes to IgG modified by neuraminidase sialidase. The existence of sialic acid depleted glomerular structures was investigated through the glomerular binding capacity of the lectin Arachis Hypogaea peanut agglutinina lectin with a highly specific affinity for galactopyranosyl galactosamine radicals that are exposed after sialic acid removal.
Another possible mechanism for the production of anti-Ig is the binding of the Fc fragment of IgG to type II receptors on the surface of group A streptococcus. This binding induces intense anti-IgG reactivity and glomerulonephritis with anti-IgG deposits, which may have nephritogenic potential Burova, et al.
Despite the variety of findings of autoimmune reactivity, the clinical relevance of these phenomena remains undefined in APSGN.
Studies by Layrisse et al. Nevertheless, the genetic characteristics that are responsible for predisposition or resistance to the disease have not been identified. Clinical and serological characteristics As previously indicated, APSGN in developed countries is now a disease of patients with chronic debilitating diseases.
Group A Strep | Post-Streptococcal Glomerulonephritis | For Clinicians | GAS | CDC
The clinical characteristics and the prognosis in these patients are different from the milder clinical course in children. In children with APSGN massive proteinuria and cardiovascular complications are rare and early mortality exceptional. The latent period between upper respiratory infection and nephritis is 7—10 days and 2—4 weeks in cases that follow skin infection.
The typical clinical presentation is of acute nephritic syndrome hematuria, edema, hypertension, and oliguria ; in a minority of cases, APSGN may be manifested by nephrotic syndrome; and in rare cases, by a rapidly progressive crescentic glomerulonephritis clinical course. Additionally determination of M serotype of organisms resulting in severe PSGN may be helpful in determining if a severe clinical course is based on the infecting organism or underlying patient characteristics.
The authors also would like to thank Mario J. Competing Interests Andrew Schwaderer has served as consultant for Allena Pharmaceuticals for a phenotype unrelated to this paper. Post-streptococcal acute glomerulonephritis in children: Changing epidemiology of acute post-streptococcal glomerulonephritis in Northeast Florida: Prognosis of acute poststreptococcal glomerulonephritis APSGN is excellent in children, when adequately diagnosed. Prognosis of acute poststreptococcal glomerulonephritis in childhood: Clinico-pathologic correlations in acute poststreptococcal glomerulonephritis.
A correlation between renal functions, morphologic damage and clinical course of 46 children with acute poststreptococcal glomerulonephritis.
Acute post-streptococcal glomerulonephritis in children of French Polynesia: Renal function during and after childhood acute poststreptococcal glomerulonephritis. Journal of the American Society of Nephrology. Group A streptococcal pharyngitis serotype surveillance in North America, — Sequencing emm-specific PCR products for routine and accurate typing of group A streptococci. Journal of Clinical Microbiology. Acute glomerulonephritis in children: Acute renal failure, hemolytic anemia, and thrombocytopenia in poststreptococcal glomerulonephritis.