Acute proliferative glomerulonephritis

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Acute proliferative glomerulonephritis
PAS stain.
SpecialtyNephrology Edit this on Wikidata
SymptomsHypertension[1]
CausesCaused by Streptococcus bacteria [2]
Diagnostic methodKidney biopsy, Complement profile[2]
TreatmentLow-sodium diet, Blood pressure management[2]
Frequency1.5 million (2015)[3]

Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney. 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 glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN).[4] It can be a risk factor for future albuminuria.[5] 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.[6] Acute glomerulonephritis resulted in 19,000 deaths in 2013, down from 24,000 deaths in 1990 worldwide.[7]

Signs and symptoms

Hematuria

Among the signs and symptoms of acute proliferative glomerulonephritis are the following:

Causes

Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritis) is caused by an infection with streptococcus bacteria, usually three weeks after infection, usually of the pharynx or the skin, given the time required to raise antibodies and complement proteins.[11][12] The infection causes blood vessels in the kidneys to develop inflammation, this hampers the renal organs ability to filter urine.[citation needed] Acute proliferative glomerulonephritis most commonly occurs in children.[12]

Pathophysiology

The pathophysiology of this disorder is consistent with an

inflammatory mediators.[2]

Complement activation is very important in acute proliferative glomerulonephritis. Apparently

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.[13]

Diagnosis

Acute Glomerulonephritis.

The following diagnostic methods can be used for acute proliferative glomerulonephritis:[2]

Clinically, acute proliferative glomerulonephritis is diagnosed following a differential diagnosis between (and, ultimately, diagnosis of) staphylococcal and streptococcal

DNAse B antibodies.[2]

Differential diagnosis

The differential diagnosis of acute proliferative glomerulonephritisis is based on the following:[citation needed]

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

Prevention

Antibiotic type

It is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early

prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis[14]

Treatment

Acute management of acute proliferative glomerulonephritis mainly consists of

ACE inhibitors may be added if blood pressure is not effectively controlled through diureses alone.[2]

Epidemiology

Acute glomerulonephritis resulted in 19,000 deaths in 2013 down from 24,000 deaths in 1990.[7]

References

  1. ^ .
  2. ^ a b c d e f g h Acute Poststreptococcal Glomerulonephritis Workup at eMedicine
  3. PMID 27733282
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  4. .
  5. .
  6. .
  7. ^ .
  8. .
  9. .
  10. .
  11. ^ Marianne Gausche-Hill, Susan Fuchs, Loren Yamamoto, American Academy of Pediatrics, American College of Emergency Physicians. "APLS: The Pediatric Emergency Medicine Resource". Jones & Bartlett Learning; 2004.
  12. ^ a b "Post-streptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-10-31.
  13. PMID 17342179
    .
  14. .

Further reading

External links