Poststreptococcal glomerulonephritis

Last updated: September 8, 2022

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Poststreptococcal glomerulonephritis (PSGN) is an acute glomerular inflammation that follows infection with nephritogenic strains of streptococci. Although most commonly seen in children following group A streptococcal tonsillopharyngitis, skin infections such as impetigo may also trigger PSGN. Individuals aged > 60 years (especially those with diabetes, malignancy, or alcohol dependency) may also be affected. Deposition of immune complexes within the glomerular basement membrane results in complement activation and subsequent damage to the glomeruli. PSGN typically manifests as nephritic syndrome with hematuria, mild proteinuria, edema, and hypertension. Evidence of recent streptococcal infection (e.g., elevated antistreptolysin O (ASO) and/or anti-DNase B titers) and low complement levels support the diagnosis. Close monitoring and supportive management of edema and hypertension are usually sufficient. Antibiotic therapy is indicated if there is evidence of active GAS infection, primarily to minimize the risk of complications and community spread. While most children recover fully, adults are more likely to develop rapidly progressive glomerulonephritis and/or end-stage kidney disease and may require long-term monitoring.

  • Bimodal age distribution; mostly affects children (between the ages of 3–12 years) and patients > 60 years of age
  • The incidence of PSGN has decreased in developed countries due to the systematic use of antibiotics and improved hygienic standards.

Epidemiological data refers to the US, unless otherwise specified.

Infection-associated glomerulonephritis can also occur following other bacterial infections (e.g., with Staphylococcus aureus, Staphylococcus epidermidis, gram-negative bacteria), viral infections, or malaria, and it can also manifest during an acute infection. [1]

Infective endocarditis is a common cause of staphylococcus infection-associated glomerulonephritis, especially amongst individuals who use intravenous drugs. [1][2]

Infection with nephritogenic strains of group A beta-hemolytic streptococciimmune complexes containing the streptococcal antigen deposit within the glomerular basement membrane; (likely involves molecular mimicry) → complement activation (↑ consumption of complement factors) → destruction of the glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome (see “Glomerular diseases” for more information)

Approx. 50% of patients remain asymptomatic.; Symptoms occur approximately 1–6 weeks following an acute infection.

General principles [1][3]

Suspect PSGN in individuals with features of nephritic syndrome and a recent history of GAS infection. [1]

Initial evaluation [1][4][5]

The following studies are typically routinely obtained in the initial workup for glomerular disease. Findings supportive of PSGN are detailed here. [3]

Evidence of preceding GAS infection [1]

PSGN typically occurs followinga GAS infection rather than during an active infection. Obtain appropriate diagnostic studies to isolate group A beta-hemolytic streptococci only if active infection is suspected. [1]

Additional studies [1]

Consider the following studies in case of diagnostic uncertainty.

In patients with decreased C3 complement levels, factor B antibody levels may help distinguish between PSGN (elevated factor B levels) and C3 glomerulopathy (normal factor B levels). A renal biopsy is indicated in individuals with low C3 levels and normal factor B antibody levels to confirm C3 glomerulopathy [9][10]

If both C3 and C4 complement levels are decreased in a patient with features of glomerulonephritis, consider other causes of immune-complex mediated glomerulonephritis. [5]

Renal ultrasound [11]

Renal biopsy [2][12]

The differential diagnoses listed here are not exhaustive.

Most cases of PSGN are self-limiting and complications of volume overload are managed with supportive treatment.

General principles [1]

Progressive renal failure suggests rapidly progressive glomerulonephritis; obtain a renal biopsy and initiate treatment promptly to prevent end-stage renal disease. [5][6]

Supportive care [1][2]

See also “Supportive care for AKI.”

Management of edema and volume overload

Antihypertensives [1][2][12]

Avoid ACE inhibitors and ARBs in patients with rapidly worsening renal function and/or sudden onset of nephrotic range proteinuria, as these medications can exacerbate AKI and hyperkalemia. [1][2]

Antibiotic therapy

Antibiotics do not affect the course of PSGN but should be administered in individuals with active GAS infection to prevent complications (e.g., abscess, rheumatic fever) and community outbreak of nephritogenic strains of S. pyogenes. [16]

Role of glucocorticoids [1][2][12]

Complications are more common in adults:

We list the most important complications. The selection is not exhaustive.

  • Recovery usually occurs within 6–8 weeks.
    • In children: restitution of kidney function in > 90% of cases
    • In some cases, urinalysis may remain abnormal for extended periods.
  • In adults, about 50% of patients suffer from persistently reduced renal function.
  1. Rodríguez-Iturbe B, Najafian B, Silva A, Alpers CE. Acute Postinfectious Glomerulonephritis in Children. Springer Berlin Heidelberg ; 2014 : p. 1-27
  2. Blaney SM, Giardino AP, Orange JS, et al.. Rudolph's Pediatrics, 23rd Edition. McGraw-Hill Education / Medical ; 2018
  3. Rovin BH, Adler SG, Barratt J, et al. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021; 100 (4): p.S1-S276. doi: 10.1016/j.kint.2021.05.021 . | Open in Read by QxMD
  4. Satoskar AA, Parikh SV, Nadasdy T. Epidemiology, pathogenesis, treatment and outcomes of infection-associated glomerulonephritis. Nat Rev Nephrol. 2019; 16 (1): p.32-50. doi: 10.1038/s41581-019-0178-8 . | Open in Read by QxMD
  5. Hebert LA, Parikh S, Prosek J, Nadasdy T, Rovin BH. Differential Diagnosis of Glomerular Disease: A Systematic and Inclusive Approach. Am J Nephrol. 2013; 38 (3): p.253-266. doi: 10.1159/000354390 . | Open in Read by QxMD
  6. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  7. VanDeVoorde RG. Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis. Pediatr Rev. 2015; 36 (1): p.3-13. doi: 10.1542/pir.36.1.3 . | Open in Read by QxMD
  8. Hahn RG, Knox LM, Forman TA. Evaluation of poststreptococcal illness.. Am Fam Physician. 2005; 71 (10): p.1949-54.
  9. Thurman JM. Complement in kidney disease: core curriculum 2015. Am J Kidney Dis. 2015; 65 (1): p.156-68. doi: 10.1053/j.ajkd.2014.06.035 . | Open in Read by QxMD
  10. Chauvet S, Berthaud R, Devriese M, et al. Anti-Factor B Antibodies and Acute Postinfectious GN in Children. JASN. 2020; 31 (4): p.829-840. doi: 10.1681/asn.2019080851 . | Open in Read by QxMD
  11. Smith RJH, Appel GB, Blom AM, et al. C3 glomerulopathy — understanding a rare complement-driven renal disease. Nature Reviews Nephrology. 2019; 15 (3): p.129-143. doi: 10.1038/s41581-018-0107-2 . | Open in Read by QxMD
  12. Lee JH, An YK, Yoo HY, et al. The Relevance between Renal Ultrasonographic Findings and Disease Course in Two Poststreptococcal Glomerulonephritis (PSGN) Patients. Child Kidney Dis. 2015; 19 (2): p.184-189. doi: 10.3339/chikd.2015.19.2.184 . | Open in Read by QxMD
  13. Balasubramanian R, Marks SD. Post-infectious glomerulonephritis. Paediatrics and International Child Health. 2017; 37 (4): p.240-247. doi: 10.1080/20469047.2017.1369642 . | Open in Read by QxMD
  14. Fogo AB, Lusco MA, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Postinfectious Glomerulonephritis. Am J Kidney Dis. 2015; 66 (4): p.e31-e32. doi: 10.1053/j.ajkd.2015.08.005 . | Open in Read by QxMD
  15. Post-streptococcal glomerulonephritis.
  16. Maness DL, Martin M, Mitchell G. Poststreptococcal Illness: Recognition and Management.. Am Fam Physician. 2018; 97 (8): p.517-522.

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