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Acute proliferative glomerulonephritis

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Title: Acute proliferative glomerulonephritis  
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Subject: Urologic disease, Kidney diseases, Microhematuria, Ureteritis, Uropathy
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Acute proliferative glomerulonephritis

Acute proliferative glomerulonephritis
Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain.
Classification and external resources
ICD-10 N00.8
ICD-9-CM 580.0
DiseasesDB 29306
MedlinePlus 000503
eMedicine med/889

Acute proliferative glomerulonephritis is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12,4 and 1 (impetigo) but also after streptococcal pharyngitis, for which it is also known as postinfectious or poststreptococcal glomerulonephritis.[1] It can be a risk factor for future albuminuria.[2] In adults, the signs and symptoms of infection may still be present at the time when the kidney problems develop, and the terms infection-related glomerulonephritis or bacterial infection-related glomerulonephritis are also used.[3] Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[4]


  • Signs and symptoms 1
  • Causes 2
  • Pathophysiology 3
  • Diagnosis 4
    • Differential diagnosis 4.1
  • Treatment 5
  • Epidemiology 6
  • References 7
  • Further reading 8
  • External links 9

Signs and symptoms

Among the signs and symptoms of acute proliferative glomerulonephritis are:


Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritisis) is caused by an infection with skin infection, the disorder occurs most often in children .[9]


The pathophysiology of this disorder is consistent with an immune complex mediated mechanism. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. As soon as binding occurs to the glomerulus, via interaction with properdin, complement is activated. Complement fixation causes the generation of additional inflammatory mediators[10]

Complement activation is very important in acute proliferative glomerulonephritis. Apparently immunoglobulin (Ig)-binding proteins bind C4BP. Complement regulatory proteins (FH and FHL-1),may be removed by SpeB, and therefore restrain FH and FHL-1 recruitment in the process of infection.[11]


Acute Glomerulonephritis.

In terms of the diagnosis of acute proliferative glomerulonephritis (poststreptococcal glomerulonephritis) can be prevented by earlyantibiotic treatment, this decision is immediate with skin infections due to the fact that the differential diagnosis is between staphylococcal and streptococcal impetigo.[12]

Via serological markers a diagnosis can be done. The streptozyme test measures different streptococcal antibodies: Antistreptolysin,Antihyaluronidase,Antistreptokinase, Antinicotinamide-adenine dinucleotidase,and Anti-DNAse B antibodies[13]

Differential diagnosis

  1. Other causes of acute glomerulonephritis:
  2. Nephrotic syndrome
  3. Other causes of generalized edema:


Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control:also a renal biopsy may be needed to be performed at some point. A low-sodium, diet may be needed when hypertension is present.In individuals with oliguric acute kidney injury, the amount of potassium should be controlled.[14]


Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[4]


  1. ^ Baltimore RS (February 2010). "Re-evaluation of antibiotic treatment of streptococcal pharyngitis". Curr. Opin. Pediatr. 22 (1): 77–82.  
  2. ^ White AV, Hoy WE, McCredie DA (May 2001). "Childhood post-streptococcal glomerulonephritis as a risk factor for chronic renal disease in later life". Med. J. Aust. 174 (10): 492–6.  
  3. ^ Nasr SH1, Radhakrishnan J, D'Agati VD (May 2013). "Bacterial infection-related glomerulonephritis in adults". Kidney Int 83 (5): 792–803.  
  4. ^ a b GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet.  
  5. ^ Sung HY, Lim CH, Shin MJ; et al. (December 2007). "A case of post-streptococcal glomerulonephritis with diffuse alveolar hemorrhage". J. Korean Med. Sci. 22 (6): 1074–8.  
  6. ^ Wilkiins, Lippincott Williams & (2015-01-16). Handbook of Signs & Symptoms. Lippincott Williams & Wilkins.  
  7. ^ a b Surgeons, American Academy of Orthopaedic; Physicians, American College of Emergency (2009-11-13). Critical Care Transport. Jones & Bartlett Learning. p. 959.  
  8. ^ Garfunkel, Lynn C.; Kaczorowski, Jeffrey; Christy, Cynthia (2007-07-05). Pediatric Clinical Advisor: Instant Diagnosis and Treatment. Elsevier Health Sciences. p. 223.  
  9. ^ "Post-streptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia". Retrieved 2015-10-31. 
  10. ^ "Acute Poststreptococcal Glomerulonephritis: Background, Pathophysiology, Epidemiology". 
  11. ^ Rodríguez-Iturbe, B.; Batsford, S. (2007-03-07). "Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet". Kidney International 71 (11): 1094–1104.  
  12. ^ Rodriguez-Iturbe, Bernardo; Musser, James M. (2008-10-01). "The Current State of Poststreptococcal Glomerulonephritis". Journal of the American Society of Nephrology 19 (10): 1855–1864.  
  13. ^ "Acute Poststreptococcal Glomerulonephritis Workup: Approach Considerations, Hematologic and Blood Chemistry Studies, Urine Studies". Retrieved 2015-10-31. 
  14. ^ "Acute Poststreptococcal Glomerulonephritis Treatment & Management: Approach Considerations, Consultations, Long-Term Monitoring". 

Further reading

  • Wilkins, Lippincott Williams & (2004-01-01). Rapid Assessment: A Flowchart Guide to Evaluating Signs and Symptoms. Lippincott Williams & Wilkins.  

External links

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