Poststreptococcal Glomerulonephritis

Post-streptococcal glomerulonephritis (PSGN) is a type of nephritis that is caused by a prior infection with group A beta-hemolytic Streptococcus (GAS). The clinical presentation of PSGN can range from asymptomatic, microscopic hematuria to full-blown acute nephritic syndrome, which is characterized by red-to-brown urine, proteinuria, edema, and acute kidney injury. The diagnosis is made based on clinical findings in the setting of recent GAS infection. Management is supportive and involves treating the clinical manifestations. The prognosis is generally favorable, especially in children.

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Poststreptococcal glomerulonephritis (PSGN) is an immunologically mediated, delayed sequela to clinical pharyngitis or skin infections caused by group A Streptococcus (GAS).


  • Age at presentation
    • Children between ages 5 and 12
    • Adults over 60 years old
  • Most common cause of acute nephritis worldwide, especially in developing countries
  • 470,000 new cases yearly
  • Annual incidence of 9.5 to 28.5 per 100,000 individuals


  • Glomerular immune complex deposition induced by specific nephritogenic strains of group A beta-hemolytic Streptococcus → triggers complement activation and inflammation (type III hypersensitivity reaction)
  • Nephritogenic strains of GAS never cause rheumatic fever.

Clinical Presentation

  • Usually occurs more than 10 days after preceding infection by group A beta-hemolytic Streptococcus
    • Strep pharyngitis
    • Scarlet fever
    • Impetigo 
  • Presentation varies:
    • Asymptomatic, microscopic hematuria (most common)
    • Acute nephritic syndrome
      • Hematuria
      • Proteinuria
      • Edema
      • Oliguria
      • Hypertension
      • Elevated serum creatinine
    • Rapidly progressive glomerulonephritis seen In 0.5% of cases


Patient’s history:

  • Recent pharyngitis 
  • Recent skin infection

Physical exam findings:

  • Hypertension
  • Edema
  • Oliguria

Lab findings:

  • Recent positive throat or skin culture for GAS infection
  • Serology tests for:
    • Antistreptolysin-O after pharyngeal infection
    • Antihyaluronidase (AHase)
    • Antinicotinamide-adenine dinucleotidase (Anti-NAD)
    • Antistreptokinase (ASKase) after skin infection
    • Anti-DNase B after skin infection
  • If only the antistreptolysin-O titer is used to screen for GAS, it may be falsely negative.
  • Urinalysis
    • Hematuria with RBC casts
    • +/- Proteinuria
  • Other tests
    • ↑ BUN and creatinine
    • ↓ C3 and CH50
    • C2 and C4 usually normal, may be decreased in some cases

Renal biopsy:

  • Indicated if there is significant renal impairment that requires dialysis
  • Findings:
    • Light microscopy
      • Diffuse endocapillary proliferation
      • Leukocytic (neutrophilic) infiltration
    • Electron microscopy
      • Primarily subepithelial immune complex deposits
      • Subendothelial deposits in early disease stages
    • Fluorescence microscopy
      • Granular IgG, complement component 3 (C3), glomerular basement membrane (GBM), and mesangium
      • Granular IgA in rare cases
Acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis:
An enlarged glomerulus with global closure of the capillary lumina caused by endogenous predominantly mesangial cell proliferation, infiltrating bloodborne monocytes, and polymorphonuclear leukocytes (H&E staining).

Image: “IgA-dominant acute poststreptococcal glomerulonephritis with concomitant rheumatic fever successfully treated with steroids: a case report” by Rus RR, Toplak N, Vizjak A, Mraz J, Ferluga D. License: CC BY 2.5



  • Supportive care
  • Antibiotics if the strep infection is still present at the time of diagnosis
    • Penicillin
    • Erythromycin if allergic to penicillin
  • Treat hypertension and/or edema
    • Loop diuretics (e.g., furosemide)
    • Sodium and water restriction
  • For hypertensive encephalopathy (rare)
    • Oral nifedipine
    • Parenteral nicardipine
  • Dialysis Indications:
    • Fluid overload that is unresponsive or slow to respond to supportive measures
    • Refractory hypertension
    • Evidence of serious compromise of renal function (rapidly rising creatinine)
    • Hyperkalemia > 6.5 mEq/L
    • Uremia with BUN of 89–100 mg/dL


  • Usually, there is rapid resolution of symptoms.
    • Hematuria usually resolves in 3 to 6 months.
    • Proteinuria usually resolves in less than 3 months.
    • Children have 95% complete recovery.
    • Adults have 60% complete recovery.
  • Recurrent episodes are rare.
  • Some patients (usually adults) progress to rapidly progressive glomerulonephritis (RPGN).
    • Develop hypertension
    • Recurrent proteinuria
    • Renal insufficiency up to 10–40 years after diagnosis

Differential Diagnosis

  • C3 glomerulonephropathy: has a clinical presentation that may be indistinguishable from PSGN. The condition also presents with hematuria, hypertension, proteinuria, and hypocomplementemia, and it may be preceded by an upper respiratory infection. Unlike with PSGN, patients with C3 glomerulonephropathy have persistent urinary abnormalities and hypocomplementemia beyond 4–6 weeks, and they occasionally have a further elevation of serum creatinine.
  • IgA nephropathy: presents with glomerulonephritis after a preceding upper respiratory infection, as PSGN can. However, there is usually a shorter time between the infection and nephritic syndrome (less than 5 days) than with PSGN. IgA nephropathy can be recurrent, and patients can have preceding episodes of gross hematuria. Management is with ACE inhibitors or angiotensin II receptor blockers, statin therapy for hyperlipidemia, and immunosuppressive therapy. Patients who progress to end-stage renal disease can be treated with dialysis or transplantation. 
  • Secondary causes of glomerulonephritis: can be seen with lupus nephritis and Henoch-Schönlein purpura (HSP). These diseases have extrarenal manifestations specific to the disease process. Henoch-Schönlein purpura does not have hypocomplementemia. Lupus nephritis has reductions in both complement component 3 and 4, while the latter is usually normal in PSGN. Diagnosis is made by renal biopsy. Management is with ACE inhibitors or angiotensin II receptor blockers, statin therapy for hyperlipidemia, anticoagulation, and immunosuppressive therapy.


  1. Kumar V, Abbas AK, Aster JC. (2015). Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders.
  2. Lewis JB & Neilson EG. (2018). Glomerular diseases. In Jameson J., et al. (Eds.). Harrison’s Principles of Internal Medicine, (20th ed.).
  3. Niaudet P. (2020). Poststreptococcal glomerulonephritis. UpToDate. Retrieved March 10, 2021, from
  4. Rodriguez-Iturbe B & Haas M. (2016). Post-streptococcal glomerulonephritis.

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