Synopsis
Recognise infection-related immune-complex glomerulonephritis, distinguish a latent post-streptococcal presentation from ongoing infection, and provide supportive renal care without missing sepsis or an alternative complement disorder.
- Infection-related glomerulonephritis may follow a resolved infection or occur while infection remains active; the latter is increasingly important in older adults, diabetes and frailty.
- Classic post-streptococcal disease follows pharyngitis after roughly one to three weeks or skin infection after about three to six weeks rather than occurring simultaneously.
- Haematuria, oedema, hypertension, reduced eGFR and variable proteinuria form the nephritic pattern; nephrotic-range protein loss can occur and does not exclude the diagnosis.
- C3 is commonly low through alternative-complement activation and usually recovers within weeks; persistent hypocomplementaemia demands reassessment for C3 glomerulopathy, lupus or ongoing infection.
- Antistreptolysin O supports recent pharyngeal streptococcal exposure, while anti-DNase B can be more helpful after skin infection; neither test alone proves renal causation.
- Staphylococcal infection-related GN may be IgA-dominant and can arise during deep infection, endocarditis, osteomyelitis or an infected device.
- Blood cultures and echocardiographic assessment are essential when endocarditis is plausible because immunosuppression before infection control can be catastrophic.
- Treatment centres on eradication of active infection and management of fluid, blood pressure, potassium and uraemia; routine glucocorticoids have no established role.
- Kidney biopsy is considered for atypical timing, severe or progressive failure, persistent complement consumption, marked proteinuria or diagnostic uncertainty.
- Recovery is often good in children but less predictable in adults with comorbidity, severe AKI or chronic histological damage, so kidney follow-up must continue after infection resolves.
Key red flags
Persistent fever, new murmur, embolic lesions, splenomegaly, weight loss or implanted cardiac material requires blood cultures and an endocarditis pathway before immune treatment.
Oedema, rising blood pressure, basal crackles and reduced urine output reflect sodium retention and may progress quickly to pulmonary oedema.
Severe headache, vomiting, confusion, visual change or seizure with marked hypertension can represent encephalopathy and requires monitored emergency treatment.
Investigation priorities
Identify glomerular haematuria, red-cell casts and the amount and character of protein loss.
Management branches
Haematuria, oedema, hypertension and AKI appear after or during an infection.
- Assess ABCDE, pulmonary oedema, blood pressure, potassium, acid–base state and urine output, treating immediate renal emergencies and involving nephrology early.
- Send microscopy, quantitative protein, complement, cultures and exposure-directed serology, and examine carefully for skin, dental, cardiac, bone, line or prosthetic infection.
- Use timing and infection status to distinguish delayed post-streptococcal disease from ongoing infection-related GN, arranging biopsy if severity or uncertainty makes histology actionable.