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Acute proliferative glomerulonephritis

  (Redirected from Post-streptococcal glomerulonephritis)

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.[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]

Acute proliferative glomerulonephritis
Post-infectious glomerulonephritis - very high mag.jpg
Micrograph of a post-infectious glomerulonephritis. Kidney biopsy. PAS stain.
Specialty Nephrology Edit this on Wikidata
Causes Caused by Streptococcus bacteria [1]
Diagnostic method Kidney biopsy, Complement profile[1]
Treatment Low-sodium diet, Blood pressure management[2]
Frequency 1.5 million (2015)[3]

Contents

Signs and symptomsEdit

 
Hematuria

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

CausesEdit

Acute proliferative glomerulonephritis (post-streptococcal glomerulonephritisis) 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.[12][13] 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.[13]

PathophysiologyEdit

The pathophysiology of this disorder is consistent with an immune-complex-mediated mechanism, a type III hypersensitivity reaction. 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, the complement is activated. Complement fixation causes the generation of additional inflammatory mediators[1]

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.[14]

DiagnosisEdit

 
Acute Glomerulonephritis.

The following diagnostic methods can be used for acute proliferative glomerulonephritis:[1]

Clinically, acute proliferative glomerulonephritis is diagnosed following a differential diagnosis between (and, ultimately, diagnosis of) staphylococcal and streptococcal impetigo. Serologically, diagnostic markers can be tested; specifically, the streptozyme test is used and measures multiple streptococcal antibodies: antistreptolysin, antihyaluronidase, antistreptokinase, antinicotinamide-adenine dinucleotidase, and anti-DNAse B antibodies.[15]

Differential diagnosisEdit

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

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

PreventionEdit

 
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,[16] while others reject that antibiotics can prevent acute proliferative glomerulonephritis.[17]

TreatmentEdit

Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control and a renal biopsy may be needed 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.[2]

EpidemiologyEdit

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

ReferencesEdit

  1. ^ a b c d "Acute Poststreptococcal Glomerulonephritis: Background, Pathophysiology, Epidemiology". 
  2. ^ a b "Acute Poststreptococcal Glomerulonephritis Treatment & Management: Approach Considerations, Consultations, Long-Term Monitoring". 
  3. ^ GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577 . PMID 27733282. 
  4. ^ Baltimore RS (February 2010). "Re-evaluation of antibiotic treatment of streptococcal pharyngitis". Curr. Opin. Pediatr. 22 (1): 77–82. doi:10.1097/MOP.0b013e32833502e7. PMID 19996970. 
  5. ^ 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. PMID 11419767. 
  6. ^ Nasr SH; Radhakrishnan J; D'Agati VD (May 2013). "Bacterial infection-related glomerulonephritis in adults". Kidney Int. 83 (5): 792–803. doi:10.1038/ki.2012.407. PMID 23302723. 
  7. ^ 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. 385: 117–71. doi:10.1016/S0140-6736(14)61682-2. PMC 4340604 . PMID 25530442. 
  8. ^ 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. doi:10.3346/jkms.2007.22.6.1074. PMC 2694628 . PMID 18162726. [permanent dead link]
  9. ^ Wilkiins, Lippincott Williams & (2015-01-16). Handbook of Signs & Symptoms. Lippincott Williams & Wilkins. ISBN 9781496310545. 
  10. ^ a b Surgeons, American Academy of Orthopaedic; Physicians, American College of Emergency (2009-11-13). Critical Care Transport. Jones & Bartlett Learning. p. 959. ISBN 9780763712235. 
  11. ^ Garfunkel, Lynn C.; Kaczorowski, Jeffrey; Christy, Cynthia (2007-07-05). Pediatric Clinical Advisor: Instant Diagnosis and Treatment. Elsevier Health Sciences. p. 223. ISBN 9780323070584. 
  12. ^ 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.
  13. ^ a b "Post-streptococcal glomerulonephritis (GN): MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-10-31. 
  14. ^ Rodríguez-Iturbe, B.; Batsford, S. (2007-03-07). "Pathogenesis of poststreptococcal glomerulonephritis a century after Clemens von Pirquet". Kidney International. 71 (11): 1094–1104. doi:10.1038/sj.ki.5002169. ISSN 0085-2538. PMID 17342179. 
  15. ^ "Acute Poststreptococcal Glomerulonephritis Workup: Approach Considerations, Hematologic and Blood Chemistry Studies, Urine Studies". emedicine.medscape.com. Retrieved 2015-10-31. 
  16. ^ 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. doi:10.1681/ASN.2008010092. ISSN 1046-6673. PMID 18667731. 
  17. ^ Allan H Goroll, Albert G Mulley, Jr. Primary Care Medicine: Office Evaluation and Management of The Adult Patient, 6th ed. Lippincott Williams & Wilkins; 2011.

Further readingEdit

External linksEdit

Classification
External resources