Poststreptococcal Glomerulonephritis

Article Author:
Prashanth Rawla
Article Editor:
Dipesh Ludhwani
2/25/2020 1:02:39 AM
PubMed Link:
Poststreptococcal Glomerulonephritis


Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys.

PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo).[1]

When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema. Less commonly presentation can mimic nephrotic syndrome with significant proteinuria.

In the US, the incidence of PSGN has declined but elsewhere the condition continues to occur at a high rate.


Nephrogenic streptococci infection precedes PSGN, which initially affects skin or oropharynx. More recently, PSGN is associated with skin infections (impetigo) more frequently than throat infections (pharyngitis).[2][3]

Rare causes of post-infectious glomerulonephritis include other bacterial or viral infections and malaria.

Poor hygiene, overcrowding, and low socioeconomic status are important risk factors for streptococci outbreaks, and this explains the higher incidence of PSGN in the impoverished countries.

Genetic factors are expected to predispose to the condition since almost 40% of patients with PSGN gave a positive family history. There is no specific gene found to cause PSGN.


Over the past three decades, PSGN incidence has significantly dropped in the developed countries; such as the United States, UK, Central Europe, and Japan. The reason for this progress is the use of antibiotic prophylaxis and the improvement of hygienic states. In these developed countries, PSGN has become more frequently seen in adult patients who suffer from chronic debilitating diseases.[4]

On the other hand, PSGN is still the most common cause of kidney injury in children in the Middle East, Africa, Australia, and worldwide. The annual incidence of new cases of PSGN in the developing countries ranges from 8.5 to 28.5 per 100000 individuals.[5] Around 97% of cases reported with PSGN live in underprivileged countries.

Clinically manifestations of PSGN are more common in males than in females with a ratio of 2:1. However; the incidence of subclinical PSGN is almost equal in both sexes. Racial factors were not found to play a role.

The disease most frequently affects children between the age of 3 and 12 (with the peak incidence between 5 to 6 years), and seniors greater than 60 years old.


The disease is immunological; representing a type III hypersensitivity reaction. The exact mechanism by which PSGN occurs is not fully determined. The body responds to nephrogenic streptococcal infection by forming immune complexes containing the streptococcal antigen with a human antibody.[6] Some theories suggest that these immune complexes become deposited in kidney glomeruli reaching through the circulation. Others claim that the condition results from an “in situ” formation of the antigen-antibody complex within the kidney glomeruli. This “In situ immune complex formation” is either due to a reaction against streptococci antigens deposited in the glomerular basement membrane or, according to other theories, due to an antibody reaction against glomerular components that cross-react with streptococcal antigen.[7]

Immune complexes formation activates complement pathway ending in the destruction of renal glomeruli.

In addition to the streptococcal antigens, some patients may also have cryoglobulins, rheumatoid factor and antineutrophilic cytoplasmic serum antibodies present.

History and Physical

Approximately 50% of children with PSGN are asymptomatic and are discovered accidentally during routine urine analysis.

Typically, patients give a history of a recent streptococcal infection such as pharyngitis, tonsillitis, or impetigo. However; some patients develop PSGN without experiencing symptoms of respiratory tract infection or pyoderma; this could result in a delay in diagnosing PSGN.[8]

The most common presenting symptom is gross hematuria as it occurs in 30 to 50% of cases with acute PSGN; patients often describe their urine as smoky, tea-colored, cola-colored, or rusty.

Oliguria occasionally presents in PSGN (usually resolves spontaneously in 1 to 2 weeks).

Puffiness of the eyelids (periorbital edema) is typical for nephritic syndrome. It is most prominent in the morning and tends to resolve at the end of the day. Generalized edema is also a common feature. Moreover, in severe cases, patients might experience respiratory distress as a result of pulmonary edema.

Patients may experience other, non-specific, symptoms like anorexia, malaise, nausea, vomiting, etc.

On examination, signs of nephritic syndrome are usually manifested such as hypertension and edema. Oliguria may occur in 30-50% of patients, which is usually indicative of severe cresentic form of the disease. The condition is transient and improves in 7-14 days.


PSGN should be suspected in all children with hypertension and heart failure, even if they don’t complain of hematuria or give a history of a preceding sore throat or pyoderma.

Laboratory investigations are the most useful in PSGN assessment.

  • Evidence of a preceding streptococcal infection is determined by measuring anti-streptolysin titer (ASO), and anti-nicotinamide-adenine dinucleotidase (anti-NAD) which tend to rise following pharyngitis. Other antibodies such as anti-DNAse B and anti-hyaluronidase (AHase) are usually elevated after both pharyngitis and skin infections. ASO titer is the most frequently used test, while the most sensitive is the streptozyme test; which includes measuring the titers of all the antibodies mentioned above.
  • Serum complement levels (C3) are usually low due to its consumption in the inflammatory reaction. Mostly, the decrease in C3 concentration occurs before serum ASO has risen.[7] Complement levels usually return to normal levels in 6-8 weeks unless the case is complicated.
  • Urine analysis: shows macroscopic or microscopic hematuria, RBC casts, mild proteinuria. Only 5% of patients with PSGN have massive proteinuria that indicates nephrotic syndrome. White blood cell casts, hyaline, and cellular casts are usually present in the urine analysis.
  • Renal Function Tests: Blood urea nitrogen (BUN) and serum creatinine typically elevate during the acute phase. These values usually return to normal later.
  • In patients with heart failure and PSGN, levels of NT-proBNP will be elevated

Histologic studies:

Renal biopsy is not recommended for diagnosing patients with PSGN and is performed only when other glomerular pathologies are suspected. Renal biopsy is indicated when:

  • Renal function is worsening
  • Patient has anuria
  • There is no latent period between the acute glomerulonephritis and streptococcal infection
  • Complement levels are normal
  • There is no rise in antistreptococcal antibodies
  • There is persistent hypertension
  • Light microscopy: all glomeruli show hypercellularity (endothelial, mesangial, and inflammatory cells). These findings are non-specific and are present in other glomerular pathologies.
  • Electron microscopy: the most characteristic finding by electron microscopy is the presence of humps; which are electron-dense deposits in the subepithelial space near the glomerular basement membrane.[9]
  • Immunofluorescence microscopy: shows deposits of IgG and C3 if the tissue sample was taken in the first 2 to 3 weeks of the disease.

Imaging studies:

  • Ultrasonography: Kidneys are enlarged only in a few patients.
  • The chest x-ray may show heart failure

Treatment / Management

PSGN is a self-limiting condition in most cases, and thus only symptomatic treatment is needed. Supportive treatment aims at controlling the complications of volume overload such as hypertension and edema, which are prominent during the acute phase of the disease.[7]

General measures:

  • Salt and water restriction is the initial step to control edema.
  • Bed rest and immobilization are recommendations in the first few days of the disease.

Pharmacological therapy:

Loop diuretics: 1mg/kg IV furosemide (maximum 40mg) is given to control edema if dietary measures are not sufficient.

Antihypertensive medications: Angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs), or calcium channel blockers (CCBs) are given to control hypertension if the blood pressure fails to return to normal after diuresis. The first two should be given with caution in patients with impaired kidney functions due to their risk of hyperkalemia.

Antimicrobials: patients with evidence of a persistent streptococcal infection should receive a course of antibiotic therapy.

Immunosuppressive therapy: There’s no evidence that immune suppression is useful in patients with PSGN.[10]However, some patients with progressive renal failure may benefit from a short course of steroids.


Dialysis is only performed when potassium and creatinine levels are critically high.

Throat cultures on the patient and family members are important. All affected members need to be treated with penicillin or erythromycin.

Differential Diagnosis

  • IgA Nephropathy: usually occurs after an upper respiratory tract infection, but it differs from PSGN in the shorter latency period it takes to appear after the episode of infection.
  • Membranoproliferative glomerulonephritis: also presents with a nephritic picture and hypocomplementemia following respiratory tract infection. Complement levels take a longer time to return to normal than in PSGN.
  • Lupus nephritis: sometimes PSGN presents with a picture similar to lupus nephritis. Laboratory testing for antibodies specific to each of the diseases can help in the diagnosis.
  • Nephrotic syndrome


PSGN has an excellent prognosis especially in children with complete recovery usually occurring within 6 to 8 weeks. In adults, around 50% of the patients continue to have reduced renal function, hypertension, or persistent proteinuria.[11][12]

Death in adults is often secondary to heart failure and renal dysfunction. Studies show that in the long term some patients may continue to have abnormalities in urine, proteinuria, and hypertension.


Complications are more likely to present in adults.  During the acute phase, congestive heart failure and azotemia are likely complications which, if not managed properly, could lead to death.

Nephrotic syndrome due to rupture of the glomerular filtration barrier and chronic renal failure are possible late complications.


  • Nephrology
  • Interventional radiology for renal biopsy

Deterrence and Patient Education

Avoidance of overcrowding and personal hygiene are important measures that patients should undertake to decrease the risk of catching streptococcal infections.

Patients with throat or skin infections should seek medical advice and get the proper antibiotic therapy if they receive confirmation of a bacterial infection.

Enhancing Healthcare Team Outcomes

Managing a case of PSGN requires cooperation between internists, nephrologists, infectious disease consultants, pharmacists, and nursing staff, functioning as an interprofessional team, to provide excellent care for their patient. PSGN patient’s fluid and salt intake, as well as urine output, should be carefully monitored by the team. The pharmacist should coordinate with the clinician to ensure that the patient is on no nephrotoxic medications and emphasize medication compliance if the patient has hypertension. The visiting nurse should encourage all close contacts and family members to undergo throat swabs to rule of an acute infection. The nurse should also weigh the patient to ensure that the edema is not worsening. In addition, renal function and potassium levels need to be closely monitored.

Consulting a nephrologist (or a pediatric nephrologist) must be sought in complicated cases. These patients need monitoring for fluid and electrolyte status at each visit. Close communication between interprofessional team members is vital to ensure good outcomes. [Level 5]

The prognosis in children is excellent but adults tend to have a protracted course with at least 30 to 50% developing renal dysfunction and hypertension.[13][14](Level V)

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