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 (ASO) and/or 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 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.
- Prior infection with group A beta-hemolytic streptococci (GAS)
- Site of infection
- In children
- In adults, the site of infection is usually not the respiratory tract.
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. 
Infection with nephritogenic strains of group A beta-hemolytic streptococci → immune 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 “” for more information)
General principles 
- The diagnosis of PSGN is typically based on confirming a preceding streptococcal infection in an individual with features of acute glomerulonephritis.
- The characteristic findings in PSGN include:
- In case of diagnostic uncertainty, consider the following to evaluate for other causes of glomerulonephritis:
Suspect PSGN in individuals with features of nephritic syndrome and a recent history of . 
Initial evaluation 
The following studies are typically routinely obtained in the initial workup for glomerular disease. Findings supportive of PSGN are detailed here. 
- Urinalysis with microscopy:
Quantification of proteinuria: typically shows non-nephrotic range proteinuria 
- Urine protein/creatinine ratio: usually < 300 mg/g 
- 0.3–3.4 g/24 hour  (less commonly obtained): usually
- BMP may reveal: 
- CBC: : may show normocytic, normochromic anemia 
- C3 complement, C4 complement levels: : classically shows ↓ C3 complement with normal C4 complement 
Evidence of preceding GAS infection 
- Antistreptococcal antibody titers
- Isolation of group A beta-hemolytic streptococci
PSGN typically occurs followinga group A beta-hemolytic streptococci only if active infection is suspected.  rather than during an active infection. Obtain appropriate diagnostic studies to isolate
Additional studies 
Consider the following studies in case of diagnostic uncertainty.
- Factor B antibody levels 
- Rheumatoid factor and cryoglobulin levels 
- ANA, ANCA, anti-GBM antibody 
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 
Renal ultrasound 
- Indications: may be obtained during a diagnostic workup of hematuria
- Findings: typically normal; may show nonspecific increased echogenicity of the renal cortex
Renal biopsy 
- Indications: (not routinely performed)
Supportive findings: proliferative glomerulopathy with immune complex deposits 
- Light microscopy: enlarged and hypercellular glomeruli
- Immunofluorescent microscopy: granular deposits in the glomerular mesangium and capillaries ; 
- Electron microscopy: immune complexes between the epithelial cell layer and the glomerular basement membrane ; (referred to as subepithelial humps) 
- See “Diseases associated with nephritic syndrome.”
- Glomerulonephritis with low serum complement levels 
- Glomerulonephritis with normal serum complement levels 
The differential diagnoses listed here are not exhaustive.
General principles 
- Consult nephrology to develop a treatment plan.
- Admit patients with any of the following indications of severe disease: 
- Manage associated symptoms (e.g., edema, hypertension) as needed.
- Treat current infection, if present.
- Monitor blood pressure, BMP, urinalysis, urine protein, and complement levels until they return to baseline. 
Supportive care 
See also “.”
Management of edema and volume overload
- Indicated for hypertension refractory to management of edema and volume overload
Preferred agents include:
- Calcium channel blockers (e.g., nifedipine)
- ACE inhibitors or ARBs
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. 
- Indication: evidence of active infection (e.g., positive cultures for ) to prevent 
- Regimens: should be based on the site of infection; follow local protocols when available.