Synopsis
Recognise the haematuria-hypertension-oedema syndrome, stabilise fluid overload and kidney injury, confirm a post-infectious pattern without premature closure, and identify features requiring urgent nephrology or biopsy.
- Acute nephritic syndrome is glomerular haematuria with variable proteinuria, hypertension, oedema, oliguria and reduced kidney function; red-cell casts strongly support glomerular bleeding.
- Post-streptococcal glomerulonephritis typically follows streptococcal pharyngitis by about 1–2 weeks or skin infection by about 3–6 weeks.
- The urine may look smoky, tea or cola coloured. Periorbital oedema is common, but the dangerous physiology is intravascular salt and water expansion with hypertension.
- First-line assessment includes blood pressure against age, sex and height centiles, neurological and respiratory examination, weight, urine output and complete fluid balance.
- First-line investigations are urinalysis and microscopy, urine protein:creatinine ratio and culture, serum creatinine and electrolytes, albumin, FBC and complement C3/C4.
- Evidence of antecedent streptococcal infection comes from ASO and anti-DNase B titres interpreted with the clinical interval; throat or skin cultures may already be negative.
- The typical complement pattern is low C3 with normal C4. Repeat C3 at 6–8 weeks; failure to normalise prompts evaluation for C3 glomerulopathy, lupus or another diagnosis.
- First-line management is supportive: salt restriction, fluid input approximately matching urine plus insensible losses, daily weight and frequent blood-pressure and renal monitoring.
- Furosemide is used for clinically important fluid overload and often improves volume-mediated hypertension; persistent hypertension may need a calcium-channel blocker under specialist direction.
- A 10-day penicillin course eradicates a remaining nephritogenic group A streptococcus and limits transmission, but it does not reverse immune-complex nephritis already established.
- Dialysis decisions are clinical and include refractory hyperkalaemia, acidosis, pulmonary oedema, uraemic complications or fluid overload, not a creatinine number alone.
- Most post-streptococcal symptoms resolve over 2–3 weeks, while microscopic haematuria can persist for 1–2 years; follow blood pressure, proteinuria, function and complement trajectory.
Key red flags
Headache, vomiting, visual change, confusion or seizure with hypertension suggests hypertensive encephalopathy and requires emergency treatment.
Breathlessness, hypoxaemia, basal crepitations, gallop rhythm or rapidly increasing weight suggests pulmonary oedema from salt and water retention.
Rapidly rising creatinine, potassium elevation, severe acidosis, oliguria or anuria requires immediate nephrology discussion and dialysis assessment.
Nephrotic-range proteinuria, marked hypoalbuminaemia, rapidly progressive function loss or systemic vasculitis features suggests a severe glomerular process beyond uncomplicated post-infectious disease.
Persistently low C3 after 6–8 weeks, low C3 and C4 together, positive ANA or ANCA, or recurrent episodes argues against a simple resolving post-streptococcal course.
A family history of kidney failure or deafness, hearing abnormalities or ocular features raises concern for inherited collagen disease.
Investigation priorities
Confirm glomerular blood, quantify protein and exclude urinary infection.
Management branches
A child has haematuria with oedema, hypertension or reduced urine.
- Measure paediatric-centile blood pressure, weight, respiratory and neurological status and establish strict fluid balance.
- Obtain urine sediment and protein quantification, renal profile, FBC, albumin, complement and streptococcal evidence.
- Admit when hypertension, oedema, AKI, oliguria, electrolyte disturbance or diagnostic uncertainty requires monitored treatment.