The PDF file you selected should load here if your Web browser has a PDF reader plug-in installed (for example, a recent version of Adobe Acrobat Reader). Analisis Faktor Risiko Glomerulonefritis Akut Pasca Streptokokus pada Anak Di RSUP Prof. Dr. R. D. Kandou Manado. Two antigenic fractions of the streptococcus (streptococcal GAPDH/nephritis- associated plasmin receptor, and streptococcal pyrogenic.

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Neuraminidase promotes neutrophil, lymphocyte and macrophage infiltration in the normal rat kidney.

Jurnal e-CliniC (eCl)

Epub Nov Hemodialysis and peritoneal dialysis may also be required to treat azotemia, hyperkalemia, or severe circulatory congestion. Immunofluorescence Microscopy Immunofluorescence findings in evolving stages of post-streptococcal GN have been elegantly defined by Sorger et al. Electron-microscopy in acute post-streptococcal GN. NAPlr is present in early biopsies of APSGN and, since it is not co-localized with complement or IgG, its role as a nephritogen is thought to be related to its glomerulonefriis capacity, which facilitates immune complex deposition glomeruulonefritis inflammation Oda, et al.

The current state of poststreptococcal glomerulonephritis. To view a copy of this license, visit http: Thiazide diuretics are ineffective and aldosterone antagonists carry the risk of hyperkalemia. Patients with an acute nephritic syndrome require restriction of sodium and fluid intake. Post-streptococcal glomerulonephritis is a strong risk factor for chronic kidney disease in later life. Nevertheless, the genetic characteristics glojerulonefritis are responsible for predisposition or resistance to the disease have not been identified.

Antibody to streptococcal zymogen in the serum of patients with acute glomerulonephritis: Clinical presentations strrptokokus proteinuria in the nephrotic range glomerulohefritis developing rapidly progressive renal failure are rare enough in APSGN that histopathological confirmation of the diagnosis is essential.


Discrepancies may partially result from the different prognosis of PSGN in adults and in children, which is not always taken into account in the reported series. Extracellular neuraminidase production of streptococci associated with acute nephritis. Evidence of lectin complement pathway activation in poststreptococcal glomerulonephritis.

Clinical and histologic resolution of poststreptococcal glomerulonephritis with large subendothelial deposits and kidney failure. Synopsis of clinical and flomerulonefritis features. Rare immune-mediated pneumonitis in association with post-streptococcal glomerulonephritis. Streptococcal exotoxin B increases interleukin-6, tumor necrosis factor alpha, interleukin-8 and transforming growth factor beta-1 in leukocytes. However, nephritis may also follow infections with group C streptococci since Str.

The Journal streptokookus Experimental Medicine. Expression of adhesion molecules in poststreptococcal glomerulonephritis. This low value is remarkably close to the estimate of Carapetis et al. The immediate prognosis is excellent in children, but adults have a significant early mortality, which partially results from cardiovascular disease.

Presently, two streptococcal antigenic fractions with substantial claims to nephritogenicity are being actively investigated. The multidimensional nature of renal disease: The plasmin-binding capacity of streptokoku antigens favors immune complex deposition and inflammation. The typical pathological changes are endocapillary proliferation with varying degrees of leukocyte infiltration, and C3, IgG, and IgM immune deposits. Current Opinion in Pediatrics. Changing perspectives in children hospitalized with poststreptococcal acute glomerulonephritis.

Follow-up of patients with epidemic poststreptococcal glomerulonephritis. Streptococcal protein H forms soluble complement-activating complexes with IgG, but inhibits complement activation by IgG-coated targets. The number of these deposits varies considerably between different cases; they can be quite segmental or rather numerous, although not so much so as to suggest a membranous nephropathy.

Erythrogenic toxin type B and its precursor isolated from nephritogenic streptococci induce leukocyte infiltration in normal rat kidneys. Deficiency of the complement factor H-related protein 5 has also been proposed as a factor that may result in a predisposition to the development of chronic renal disease Vernon, et al.


Post-Streptococcal Glomerulonephritis – Streptococcus pyogenes.

Post-Streptococcal Glomerulonephritis – Streptococcus pyogenes – NCBI Bookshelf

Subtypes of acute postinfectious glomerulonevritis. Alterations of cell adhesion molecules in human glomerular endothelial cells in response to nephritis-associated plasminogen receptor. The global burden of group A streptococcal diseases. Review Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet. Role of intrarenal vascular sclerosis in progression of poststreptococcal glomerulonephritis.

The pathogenesis of a laboratory model resembling the spectrum of human glomerulonephritis. Epub Oct Journal of Clinical Microbiology. Notably, in studies of the Str. Several mechanisms may participate in the pathogenesis of renal damage Table 1. The current spectrum of infectious glomerulonephritis. The Medical Journal of Australia.

The best markers for nephritogenic streptococcal infection are serum antibody levels to NALPr Yamakami, et al. Investigation of milk-borne Streptococcus zooepidemicus infection associated with glomerulonephritis in Australia. In the acute phase of the disease, interstitial inflammation, which is typically comprised of a mixture of lymphocytes, monocytes, plasma cells, and neutrophils, is present in most cases. In a recent study of a specific outbreak of PSGN that resulted from the consumption of cheese contaminated with Streptococcus zooepidemicus and that affected mostly adults, there was an alarming incidence of chronic renal disease: Determining antibody-binding site of streptococcal pyrogenic exotoxin B to protect mice from group a streptococcus infection.

The Journal of Clinical Investigation. Work by Fujino et al.