Poststreptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia
induce glomerulonephritis and rheumatic fever as late complications [1, 2]. The relationship between acute glomerulonephritis and infections with GAS was time of discharge a throat culture was positive for beta-hemolytic streptococci, Lance. Poststreptococcal glomerulonephritis is one of the oldest recognized renal diseases. especially in association with debilitating conditions such as alcoholism or early antibiotic treatment of streptococcal infections in index cases of PSGN. . blood leukocytes respond with release of IL-6, TNF-α, IL-8, and TGF-β when. this period that the relation between streptococcal of skin infection and AGN developed largely as a tative results of beta 1-C/beta 1-A-globulin levels in.
Abstract Acute glomerulonephritis that results from streptococcal infections is the best-studied immune complex-mediated glomerulonephritis. Initially described in the convalescence of scarlet fever, the incidence of acute post streptococcal glomerulonephritis APSGN has decreased worldwide, particularly in developed countries where it is now rare and is limited to adult patients who have debilitating conditions. In developing countries, the annual burden of APSGN remains at a level of least 9 cases perinhabitants.
Glomerulonephritis results from the glomerular deposition of circulating immune complexes and by the in situ formation of immune complexes.
In-situ formation of immune complexes is a characteristic associated with cationic antigens that have a charge-facilitated penetration through the polyanionic glomerular basement membrane. The plasmin-binding capacity of streptococcal 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. The immediate prognosis is excellent in children, but adults have a significant early mortality, which partially results from cardiovascular disease. The long-term development of end-stage renal disease is exceptional in children. However, studies in aboriginal communities indicate that patients with a history of APSGN have a higher incidence of albuminuria, and that APSGN represents a risk factor for the subsequent development of chronic renal failure, if associated with diabetes and obesity.Group A Streptococcus (GAS): Symptoms & Other Clinical Features – Infectious Diseases - Lecturio
Introduction Acute poststreptococcal glomerulonephritis APSGN is the prototype of post-infectious glomerulonephritis and is associated with a previous skin or throat infection by group A streptococcus Streptococcus pyogenesor occasionally groups C or G streptococcus. This landmark paper opened the field of immune complex-mediated diseases. Epidemiology APSGN may occur in epidemic outbreaks or in clusters of cases, and it may occur in isolated patients.
The most recent epidemics have occurred in the indigenous communities of the Northern Territory of Australia, resulting from pyoderma after infection with emm55 group A streptococcus Marshall, et al. Streptococcus zooepidemicus has also caused clusters of cases 5—15 patients reported in the last two decades in poor communities in industrialized countries Nicholson, et al. The reduction of the incidence of APSGN is probably the result of easier and earlier access to appropriate medical care for streptococcal infections.
Reports from France Simon, et al.
Post-Streptococcal Glomerulonephritis - Streptococcus pyogenes - NCBI Bookshelf
We assumed that the cases of acute glomerulonephritis were in fact APSGN, which was explicitly stated in most series, but not in all. These patients had severe renal failure because they were seen at a referral hospital and admitted to the intensive care unit, if one was available, and then dialyzed.
The total number of cases in the general population was estimated, considering that uncomplicated cases of APSGN are to times more common than those of life-threatening disease.
This low value is remarkably close to the estimate of Carapetis et al. Several mechanisms may participate in the pathogenesis of renal damage Table 1. Nephritogenic immune complexes are formed in circulation and deposited in the glomeruli; alternately, the antigen and antibody arrive separately and meet in or outside the glomerular basement membrane, causing in situ immune complex disease.
Immune cell recruitment, production of chemical mediators and cytokines, and local activation of the complement and coagulation cascades drive an inflammatory response that is localized in the glomeruli. Glomerular deposition of circulating immune complexes depends on the antigen load, the antigen: In situ formation of immune complexes is favored by cationic antigens that have a charge-dependent facilitated penetration into the polyanionic glomerular basement membrane, and tend to occur in conditions of antigen excess Vogt, et al.
Pathogenetic mechanisms participating in acute poststreptococcal glomerulonephritis Nephritogenic antigens Traditionally, APSGN was considered to be caused by an antigen present in group A streptococci. Streptococcus pyogenes of M types 1, 2, 4, and 12 were associated with epidemic nephritis resulting from upper respiratory infections and M types 47, 49 and 55 were associated with epidemic nephritis following pyoderma.
However, nephritis may also follow infections with group C streptococci since Str. The nephritogenic potential of streptokinase was investigated by Nordstrand et al. Presently, two streptococcal antigenic fractions with substantial claims to nephritogenicity are being actively investigated.
Work by Fujino et al. However, people mostly commonly spread group A strep through direct person-to-person transmission. Typically transmission occurs through saliva or nasal secretions from an infected person.
- Post-Streptococcal Glomerulonephritis
Symptomatic people are much more likely to transmit the bacteria than asymptomatic carriers. Crowded conditions — such as those in schools, daycare centers, or military training facilities — facilitate transmission. Although rare, spread of group A strep infections may also occur via food. Foodborne outbreaks of pharyngitis have occurred due to improper food handling. Fomites, such as household items like plates or toys, are very unlikely to spread these bacteria. Humans are the primary reservoir for group A strep.
There is no evidence to indicate that pets can transmit the bacteria to humans. PSGN is more common in children, although it can occur in adults. Pharyngitis-associated PSGN is most common among children of early school age. Pyoderma-associated PSGN is most common among children of pre-school age. There are no known risk factors specific for PSGN. However, the risk of PSGN is increased if a nephritogenic strain of group A strep is introduced into a household. Diagnosis and Testing The differential diagnosis of PSGN includes other infectious and non-infectious causes of acute glomerulonephritis.
Poststreptococcal glomerulonephritis (GN)
Clinical history and findings with evidence of a preceding group A strep infection should inform a PSGN diagnosis. Evidence of preceding group A strep infection can include1 Isolation of group A strep from the throat Isolation of group A strep from skin lesions Elevated streptococcal antibodies Treatment Treatment of PSGN focuses on managing hypertension and edema.
Additionally, patients should receive penicillin preferably penicillin G benzathine to eradicate the nephritogenic strain.