Poststreptococcal Acute Glomerulonephritis: Difference between revisions
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PSAGN is the tmost common form of immune mediated inflamation of glomerules in childhood. It is caused by ''Streptococcus pyogenes'' infection.
'''PSAGN is the most common form of immune mediated inflammation of glomerules in childhood. It is caused by ''Streptococcus pyogenes'' infection.'''


== Epidemiology and Ethiology ==
== Epidemiology and Etiology ==
Typical '''age is 2-12 years'''. Patients usually have straptococcal '''pharyngitis or impetigo 5-21 days before''' PSAGN manifestation. Incidence is 6–20:100 000 in western countries (usually sporadic occurrence), in developing countries even higher because of '''lower hygienic standard''' and '''malnutrition''' (epidemic occurrence). Other risk factors are:
Typical '''age is 2-12 years'''. Patients usually have streptococcal '''pharyngitis or impetigo 5-21 days before''' PSAGN manifestation. Incidence is 6–20:100 000 in western countries (usually sporadic occurrence), in developing countries even higher because of '''lower hygienic standard''' and '''malnutrition''' (epidemic occurrence). Other risk factors are:
* gender (more frequent in '''boys''');
* gender (more frequent in '''boys''');
* even '''genetic predisposition''' for PSAGN.
* even '''genetic predisposition''' for PSAGN.
Line 10: Line 10:


== Pathophysiology ==
== Pathophysiology ==
there are some antigenes produced by ''Streptococcus pyogenes'' the most important is NSAP-streptokinase (nephritogen strains associated protein), M-protein and endostreptosin. These antigenes are binded by specific antibodies. So creaed immunocomplexes are taken up in capillaries of glomerules as deposites. It is mediated by activation of complement too. Finally, it leads to proligerative glomerulonephritis with decreased glomelural filtration, higher natrium resorption in tubules (→ edema), increased renin secretion (→ hypertension).
There are some antigenes produced by ''Streptococcus pyogenes'' the most important is NSAP-streptokinase (nephritogen strains associated protein), M-protein and endostreptosin. These antigenes are binded by specific antibodies. So creaed immunocomplexes are taken up in capillaries of glomerules as deposites. It is mediated by activation of complement too. Finally, it leads to proligerative glomerulonephritis with decreased glomelural filtration, higher natrium resorption in tubules (→ edema), increased renin secretion (→ hypertension).
 
[[File:Renal corpuscle.svg|thumb|Scheme of normal renal corpuscle.]]
[[File:Acute Glomerulonephritis Pathology Diagram.svg|thumb|Scheme of glomerular capillary in PSAGN - immune complex deposits below the podocyte foot processes (black).]]
[[File:Post-infectious glomerulonephritis - very high mag.jpg|thumb|PSAGN - histopathology.]]
== Diagnostic ==
== Diagnostic ==
=== Symptomes ===
=== Symptoms<ref>{{Cite
| type = book
| surname1 = Kliegman
| name1 = Robert M
| others = yes
| title = Nelson Essentials of Pediatrics
| edition = 5th
| location = Philadelphia
| publisher = Elseiver
| year = 2006
| pages = 758
| isbn = 978-1-4160-0159-1
}}</ref> ===
* '''edema''' (75% of patients);
* '''edema''' (75% of patients);
* '''gross hematuria''' (65%) - tea colored or cola colered urine;
* '''gross hematuria''' (65%) - tea colored or cola colored urine;
* '''hypertension''' (50%);
* '''hypertension''' (50%);
* acute renal insufficiency with oliguria.
* acute renal insufficiency with oliguria.
Line 24: Line 38:


=== Diagnostic Methods ===
=== Diagnostic Methods ===
* urine examination → hematuria, mild to moderate proteinuria, concentrated urine (there is oliguria!), and the presence of casts.
* '''urine examination''' →  
* blood examination → elevated creatinin (decreased glomerular filtration), ASLO,  
** [[hematuria]],  
*  
** mild to moderate proteinuria,  
*  
** concentrated urine (there is oliguria!),  
** and the presence of casts,
** urine culture is necessary too
* '''blood examination''' →  
** elevated creatinin (based on decreased glomerular filtration),  
** ASO antibodies,  
** reduced serum C3 level (if it has normal level, it should be different diagnosis),
** elevated serum IgM and IgG
* '''ultrasonography of kidneys'''
* renal biopsy is not indicated! -diagnosis is based on previous streptococcal infection anamnesis and symptomatology (edema, hematuria, hypertension)
 
== Therapy ==
== Therapy ==
Therapy of PSAGN is based on:
* dietary sodium restriction
* diuretics
* antihypertensive agents.
Complete remission is in 95% of patients, only 5% of all patients can progress to end stage renal disease.


<noinclude>
<noinclude>
== Links ==
== Links ==
=== Related articles ===
=== Related articles ===
* [[Nephrotic Syndrome in Children]]
* [[Proteinuria in Children]]
=== References ===
=== References ===
<references />
<references />
=== Bibliography ===
=== Bibliography ===
* {{Cite
| type = book
| surname1 = Kliegman
| name1 = Robert M
| others = yes
| title = Nelson Essentials of Pediatrics
| edition = 5th
| location = Philadelphia
| publisher = Elseiver
| year = 2006
| pages = 757-759
| isbn = 978-1-4160-0159-1
}}
* {{Cite
| type = web
| corporation = WikiSkripta
| url = http://www.wikiskripta.eu/index.php/Akutn%C3%AD_glomerulonefritida
| source_name = Akutní glomerulonefritida
| year = 2011
| date_of_revision = 2011-10-03
| cited = 2011-12-21
}}
</noinclude>
</noinclude>
[[Category:Paediatrics]]
[[Category:Paediatrics]]
[[Category:Nephrology]]

Latest revision as of 05:36, 18 March 2015

PSAGN is the most common form of immune mediated inflammation of glomerules in childhood. It is caused by Streptococcus pyogenes infection.

Epidemiology and Etiology[edit | edit source]

Typical age is 2-12 years. Patients usually have streptococcal pharyngitis or impetigo 5-21 days before PSAGN manifestation. Incidence is 6–20:100 000 in western countries (usually sporadic occurrence), in developing countries even higher because of lower hygienic standard and malnutrition (epidemic occurrence). Other risk factors are:

  • gender (more frequent in boys);
  • even genetic predisposition for PSAGN.

Nephritogenic beta-heamolytic streptococcus, group A, type M 12 and 49 ist the most often originator.

Pathophysiology[edit | edit source]

There are some antigenes produced by Streptococcus pyogenes the most important is NSAP-streptokinase (nephritogen strains associated protein), M-protein and endostreptosin. These antigenes are binded by specific antibodies. So creaed immunocomplexes are taken up in capillaries of glomerules as deposites. It is mediated by activation of complement too. Finally, it leads to proligerative glomerulonephritis with decreased glomelural filtration, higher natrium resorption in tubules (→ edema), increased renin secretion (→ hypertension).

Scheme of normal renal corpuscle.
Scheme of glomerular capillary in PSAGN - immune complex deposits below the podocyte foot processes (black).
PSAGN - histopathology.

Diagnostic[edit | edit source]

Symptoms[1][edit | edit source]

  • edema (75% of patients);
  • gross hematuria (65%) - tea colored or cola colored urine;
  • hypertension (50%);
  • acute renal insufficiency with oliguria.

consequences of hypertension, oliguria and renal insufficiency can be"

  • heart failure;
  • encephalopathy.

Diagnostic Methods[edit | edit source]

  • urine examination
    • hematuria,
    • mild to moderate proteinuria,
    • concentrated urine (there is oliguria!),
    • and the presence of casts,
    • urine culture is necessary too
  • blood examination
    • elevated creatinin (based on decreased glomerular filtration),
    • ASO antibodies,
    • reduced serum C3 level (if it has normal level, it should be different diagnosis),
    • elevated serum IgM and IgG
  • ultrasonography of kidneys
  • renal biopsy is not indicated! -diagnosis is based on previous streptococcal infection anamnesis and symptomatology (edema, hematuria, hypertension)

Therapy[edit | edit source]

Therapy of PSAGN is based on:

  • dietary sodium restriction
  • diuretics
  • antihypertensive agents.

Complete remission is in 95% of patients, only 5% of all patients can progress to end stage renal disease.


Links[edit | edit source]

Related articles[edit | edit source]

References[edit | edit source]

  1. KLIEGMAN, Robert M, et al. Nelson Essentials of Pediatrics. 5th edition. Philadelphia : Elseiver, 2006. pp. 758. ISBN 978-1-4160-0159-1.

Bibliography[edit | edit source]

  • KLIEGMAN, Robert M, et al. Nelson Essentials of Pediatrics. 5th edition. Philadelphia : Elseiver, 2006. pp. 757-759. ISBN 978-1-4160-0159-1.