Clinical presentation
CLASSIC PSGN (post-streptococcal):
- Children aged 4-12
- 1-3 weeks after Group A strep throat (Streptococcus pyogenes)
- 3-6 weeks after impetigo / skin strep
- Sudden onset: macroscopic haematuria ('cola-coloured urine'), facial and lower-limb oedema
- Hypertension, sometimes severe
- Reduced urine output, AKI in 25-40%
- Low C3 (consumed via alternative pathway); C4 usually normal
ADULT POST-INFECTIOUS GN (modern UK pattern):
- Older adults, often >50, often diabetic
- Following: skin and soft tissue infection (cellulitis, abscess), infective endocarditis, deep abscess, prosthetic infection, dialysis line infection, MRSA infection
- Often staphylococcal — IgA-dominant subtype
- Active infection still present at presentation (not a 'post' event)
- AKI, nephrotic-range proteinuria, hypertension
- Worse prognosis: 30-50% progress to CKD or ESKD
Other Triggers
- Viral: hepatitis B/C, HIV, EBV, CMV, parvovirus, COVID-19
- Parasitic: malaria, schistosomiasis, leishmaniasis (more in tropical countries)
- Fungal: rare, in immunocompromised
Investigations
Infection Screen
- Throat swab and skin swabs
- Blood cultures × 3 (think endocarditis)
- Anti-streptolysin O titre (ASOT) — rises after strep throat
- Anti-DNase B — rises after skin strep (better marker for impetigo-related PSGN)
- Echocardiogram if cardiac signs or murmur
- Imaging for deep abscess if clinically suspected
- Hepatitis B/C, HIV serology
Immunology
- C3 — LOW (consumed); usually normalises within 8 weeks
- C4 — usually normal
- ANA, ANCA, anti-GBM (rule out other causes)
- Cryoglobulins
- Serum free light chains (older adults)
Urine
- Active sediment: dysmorphic red cells, red cell casts
- Proteinuria (variable — sub-nephrotic in PSGN, can be nephrotic-range in staph-GN)
BIOPSY — when indicated (adults, atypical, persistent or progressive):
- Light microscopy: diffuse endocapillary proliferation, neutrophil infiltration
- Immunofluorescence:
- PSGN: granular IgG + C3 ('starry sky' or 'garland')
- Staphylococcal IgA-dominant GN: dominant IgA + C3 (mimics IgA nephropathy)
- Electron microscopy: large subepithelial 'humps'
When To Biopsy
- All adults with suspected post-infectious GN
- Children if: persistent C3 low >12 weeks, prolonged AKI, nephrotic syndrome, atypical features
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Treatment
Treat The Infection
- Antibiotics tailored to the organism
- Strep: penicillin V or amoxicillin
- Staph: flucloxacillin or vancomycin (MRSA)
- Source control: drainage of abscess, removal of infected hardware, valve surgery for endocarditis
SUPPORTIVE — for the kidney injury:
- Fluid and salt restriction
- Loop diuretic (furosemide) for fluid overload
- Antihypertensives — calcium channel blocker or ACE/ARB (after AKI resolved)
- Dialysis if needed (rarely required in PSGN, more often in adult staphylococcal GN)
- Treat hyperkalaemia
Immunosuppression
- Not routine
- Reserved for severe crescentic disease on biopsy (>50% crescents) — pulse methylprednisolone ± cyclophosphamide or rituximab
- Caution: only after active infection controlled
Monitoring
- Urine ACR/PCR at 6 and 12 weeks
- eGFR weekly initially, then monthly
- C3 — expect normalisation within 8 weeks; persistently low C3 should prompt re-evaluation for C3 glomerulopathy or lupus
- BP
- Long-term follow-up — particularly adults
Prognosis
CHILDREN (classical PSGN):
- Excellent — >95% recover normal kidney function
- Microscopic haematuria can persist for 1-2 years
- Mild proteinuria can persist for 5+ years
- Rare late progression to CKD
Adults
- PSGN (rare now in UK): ~50% full recovery, ~50% have residual proteinuria or CKD
- Staphylococcal IgA-dominant GN: 30-50% progress to CKD or ESKD
- Diabetes, age >65, and crescentic biopsy worsen outcome
Long-term
- Any patient with residual proteinuria or hypertension needs nephrology follow-up
- Start ACE/ARB if persistent proteinuria
- Address cardiovascular risk
- Recurrence of PSGN is rare due to immunity against the specific M-type strep
KEY MESSAGE: post-infectious GN is no longer just a paediatric problem. In adults — especially older diabetics — staphylococcal IgA-dominant GN is now the typical presentation, and outcomes are far worse.






