acute poststreptococcal glomerulonephritis

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Acute Poststreptococcal Glomerulonephritis



Acute poststreptococcal glomerulonephritis (APSGN) is an inflammation of the kidney tubules (glomeruli) that filter waste products from the blood, following a streptococcal infection such as strep throat. APSGN is also called postinfectious glomerulonephritis.


APSGN develops after certain streptococcal bacteria (group A beta-hemolytic streptococci) have infected the skin or throat. Antigens from the dead streptococci clump together with the antibodies that killed them. These clumps are trapped in the kidney tubules, cause the tubules to become inflamed, and impair that organs' ability to filter and eliminate body wastes. The onset of APSGN usually occurs one to six weeks (average two weeks) after the streptococcal infection.
APSGN is a relatively uncommon disease affecting about one of every 10,000 people, although four or five times that many may actually be affected by it but show no symptoms. APSGN is most prevalent among boys between the ages of 3 and 7, but it can occur at any age.

Causes and symptoms

Frequent sore throats and a history of streptococcal infection increase the risk of acquiring APSGN. Symptoms of APSGN include:
  • fluid accumulation and tissue swelling (edema) initially in the face and around the eyes, later in the legs
  • low urine output (oliguria)
  • blood in the urine (hematuria)
  • protein in the urine (proteinuria)
  • high blood pressure
  • joint pain or stiffness


Diagnosis of APSGN is made by taking the patient's history, assessing his/her symptoms, and performing certain laboratory tests. Urinalysis usually shows blood and protein in the urine. Concentrations of urea and creatinine (two waste products normally filtered out of the blood by the kidneys) in the blood are often high, indicating impaired kidney function. A reliable, inexpensive blood test called the anti-streptolysin-O test can confirm that a patient has or has had a streptococcal infection. A throat culture may also show the presence of group A beta-hemolytic streptococci.

Key terms

Streptococcus — A gram-positive, round or oval bacteria in the genus Streptococcus. Group A streptococci cause a number of human diseases including strep throat, impetigo, and ASPGN.


Treatment of ASPGN is designed to relieve the symptoms and prevent complications. Some patients are advised to stay in bed until they feel better and to restrict fluid and salt intake. Antibiotics may be prescribed to kill any lingering streptococcal bacteria, if their presence is confirmed. Antihypertensives may be given to help control high blood pressure and diuretics may be used to reduce fluid retention and swelling. Kidney dialysis is rarely needed.


Most children (up to 95%) fully recover from APSGN in a matter of weeks or months. Most adults (up to 70%) also recover fully. In those who do not recover fully, chronic or progressive problems of kidney function may occur. Kidney failure may result in some patients.


Receiving prompt treatment for streptococcal infections may prevent APSGN.



Fauci, Anthony S., et al., editors. Harrison's Principles of Internal Medicine. New York: McGraw-Hill, 1997.


American Kidney Fund (AKF). Suite 1010, 6110 Executive Boulevard, Rockville, MD 20852. (800) 638-8299.
National Kidney Foundation. 30 East 33rd St., New York, NY 10016. (800) 622-9010.

a·cute glo·mer·u·lo·ne·phri·tis

glomerulonephritis that frequently occurs as a late complication of pharyngitis or skin infection, due to a nephritogenic strain of β-hemolytic streptococci, characterized by abrupt onset of hematuria, edema of the face, oliguria, and variable azotemia and hypertension; the renal glomeruli usually show cellular proliferation or infiltration by polymorphonuclear leukocytes.

acute poststreptococcal glomerulonephritis

Glomerular inflammation which follows infection—e.g., pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

More common in males age 3 to 7.
Clinical findings
Acute onset of oedema, hematuria, proteinuria, and hypertension.

Lysed bacteria plug renal tubules causing inflammation.
Haematuria, proteinuria, increased ASO.
Symptomatic; bed rest, antibiotics; antihypertensives.

Paediatric Nephrologist should be consulted for:
Severe hypertension;
Severe oliguria;
Severe oedema;
Nephrotic-range proteinuria;
Azotemia if moderate or sever;
Recurrent episodes of gross haematuria;
Persistently depressed C3 (past 8-10 week).

acute poststreptococcal glomerulonephritis

Post-infectious glomerulonephritis Nephrology Glomerular inflammation which follows streptococcal infection–eg strep throat with group A beta-hemolytic streptococci Epidemiology More common in ♂ age 3 to 7 Clinical Edema of face, extremities, oliguria, proteinuria, HTN, joint pain Lab Hematuria, proteinuria, ↑ ASO Management Symptomatic; bed rest, antibiotics; antihypertensives. See Strep throat.
References in periodicals archive ?
There were focal subepithelial electron dense deposits found in the mesangial notch on electron microscopy (Figure 4) suggesting resolved post-infectious glomerulonephritis; however no active glomerulonephritis or IgA nephropathy was present.
Follow-up study of post-infectious glomerulonephritis in adults: analysis of predictors of poor outcome.
Other common glomerular disorders are membranous nephropathy (12%), IgA nephropathy (9%), and post-infectious glomerulonephritis (6%).
Post-infectious Glomerulonephritis (PIGN)###12 (6)###9 (8)###3 (3)
Other less common causes include nephrolithiasis, sickle cell disease/trait, coagulopathy, glomerular disease (including post-infectious glomerulonephritis and IgA nephropathy), malignancies (e.g., Wilms' tumour), and drug-induced hemorrhagic cystitis, such as is seen with cyclophosphamide.
Post-infectious glomerulonephritis presenting as acute renal failure in a patient with Lyme disease.
The most commonly acquired kidney diseases in children are post-infectious glomerulonephritis, nephrotic syndrome and diarrhoea-associated haemolytic uraemic syndrome.
Renal biopsy specimens showed increased mesangial cellularity, inflammatory infiltrate including neutrophils and narrowing of capillary lumina, all suggestive of post-infectious glomerulonephritis. The presence of 1gM antibody against hepatitis A virus identified it as the cause of the acute hepatitis in this patient.
Post-Infectious Glomerulonephritis (PIGN) is the commonest form of acute glomerulonephritis in developing countries, which results from immunological events triggered by many infective agents.
Post-Infectious Glomerulonephritis (PIGN) was defined as presence of features of acute nephritic syndrome and evidence of an infectious aetiology, e.g.
There were 70 cases of Acute Post-Infectious Glomerulonephritis (APIGN) in the study period of three years.
The spectrum of pathological lesions in the adult nephrotic population was wide and comprised focal and segmental glomerulosclerosis (39.87%), followed by membranous nephropathy (26.58%), minimal change disease (14.82%), mesangiocapillary glomerulonephritis (4.3%), mesangio-proliferative glomerulonephritis (4.11%), post-infectious glomerulonephritis (2.84%), IgA nephropathy (2.53%), and other rare lesions8.

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