Post-Streptococcal Glomerulonephritis

Written 27th August 2020 - Last Update 21st August 2026

Post-Streptococcal Glomerulonephritis (PSGN)

A form of nephritic syndrome — post-infectious GN (PIGN) following infection with nephritogenic strains of group A β-haemolytic Streptococcus.

Epidemiology

  • The most common cause of a glomerular disorder in children aged 5–15 (rare under 2, uncommon in adults over 40)
  • More common in Indigenous communities — the same nephritogenic-strain streptococcal infections that drive PSGN also drive the much higher acute rheumatic fever/rheumatic heart disease burden seen in the same populations, particularly in crowded or remote-community settings
  • ~5–10% of streptococcal pharyngitis and ~25% of impetigo cases progress to PIGN
  • Typical latency after streptococcal pharyngitis is 1–2 weeks; after a skin infection (impetigo) it is longer, up to 6 weeks — the two have distinctly different latency periods, not a uniform ~7–10 days for both
  • Annual incidence in developing countries is 8.5–28.5 per 100,000; incidence has fallen substantially in developed countries with better antibiotic access and hygiene, and staphylococcal infection–associated GN has now overtaken PSGN as the leading cause of infection-related GN in adults in the Western world — worth keeping in the differential for an older adult with a nephritic picture and an unclear or ongoing (rather than resolved) infection.

Nearly 90% of Australian acute rheumatic fever cases and 70% of rheumatic heart disease diagnoses occur in Aboriginal and Torres Strait Islander people — the shared population risk pattern worth keeping in mind alongside PSGN in these communities.

Clinical features

Ranges from asymptomatic haematuria (~50% of cases) and mild proteinuria, to full nephritic syndrome:

  • Irritable, lethargic, unwell child
  • Haematuria (may be dark, cola-coloured, brown or smoky) — gross haematuria in 30–50% of cases
  • Periorbital ± leg/scrotal oedema (65–90% of cases; generalised oedema suggests more severe disease)
  • Oliguria
  • Hypertension (up to 80% of cases, usually resolving within ~10 days)
  • Proteinuria (occasionally nephrotic-range)

Typical course: a few days of oliguria → hypertension/oedema for 2–4 days → resolution within 1–2 weeks. Prognosis is generally good.

Diagnosis

  • Streptococcal serology: anti-streptolysin O (ASO) titre, anti-DNase B, anti- hyaluronidase — all provide evidence of recent infection
  • Urinalysis + phase-contrast microscopy: dysmorphic red cells, red cell casts, proteinuria, WBCs, renal tubular cells
  • Hypocomplementaemia is common — C3 and CH50 fall during active disease and normalise within 6–8 weeks in ~80% of cases
  • Biopsy confirms the diagnosis but is rarely necessary — reserve it for atypical presentations: persistently low complement or no rise in streptococcal antibody titres, or a clinical/laboratory picture suggesting rapidly progressive glomerulonephritis

Management

Primarily supportive: dietary protein/sodium/fluid restriction, and treatment of oedema/hypertension in more significant cases. Dialysis is occasionally needed.

Once glomerulonephritis has developed, antibiotics do not alter its course — the infection has usually already resolved by the time kidney injury manifests, so treatment is supportive, not antimicrobial. Prophylactic antibiotics for close contacts can be considered in high-prevalence/high-transmission settings, but current evidence does not show a significant reduction in the risk of a contact then developing PSGN themselves — treating early mainly limits further spread of the nephritogenic strain, not the individual’s own risk once exposed. There is no definite role for immunosuppression; corticosteroids may have a role in severe cases to dampen acute inflammation and reduce the risk of long-term kidney damage, but this is not routine practice.

Prognosis

  • 85–95% of patients regain or retain normal renal function
  • GFR normalises over 1–3 months; proteinuria may persist 6–12 months, microscopic haematuria for several years
  • 10% of adults and 1% of children progress to rapidly progressive glomerulonephritis
  • Kidney outcomes are worse in adults than children — residual hypertension or chronic kidney disease is noted in 30–50% of affected adults, versus near-complete recovery in most children