Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Acute nephritic syndrome and post-streptococcal disease
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Hypertensive, hyperkalaemic or oliguric emergency
Pulmonary oedema, encephalopathy, seizure, severe hypertension, rapidly rising creatinine, hyperkalaemia, severe acidosis, oliguria or anuria can complicate acute glomerulonephritis and may require kidney replacement therapy.
Action: Admit, obtain senior paediatric and nephrology help immediately, use continuous physiological monitoring, establish accurate weight and fluid balance, check ECG, renal profile and blood gas, and treat life-threatening potassium, blood-pressure, respiratory and fluid complications through paediatric emergency protocols. Do not give unmeasured fluid boluses to an overloaded child.
Overview
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.
Nephritic syndrome describes inflammatory glomerular injury rather than one disease. Capillary-wall disruption permits red cells and protein into urine, while filtration falls and sodium is retained, producing oliguria, oedema and hypertension.
Post-infectious glomerulonephritis is the commonest childhood cause. Nephritogenic streptococcal antigens trigger immune-complex and complement activation after the infection has begun resolving, explaining the latent interval rather than simultaneous throat symptoms and haematuria.
The post-pharyngeal interval is usually shorter than after impetigo. By contrast, IgA nephropathy often produces visible haematuria within days of a respiratory infection, and IgA vasculitis adds palpable purpura, abdominal or joint involvement.
Ask about sore throat, scarlet-fever symptoms, skin sores, recent antibiotics, exact interval, visible urine colour, output, oedema, weight gain, headache, visual symptoms, breathlessness, rash, joints, medicines, family renal disease and hearing loss.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Complement follow-up
A child has a typical post-streptococcal nephritic syndrome with low C3 and normal C4. Which follow-up result most strongly challenges the diagnosis?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Examine blood pressure with the correct cuff and paediatric centile, perfusion, respiratory signs, heart sounds, liver, oedema and neurological status. Look for impetigo, pharyngitis, vasculitic rash and systemic lupus features.
Urinalysis usually shows blood and protein. Microscopy may reveal dysmorphic red cells and red-cell casts. Quantify protein because nephrotic-range loss predicts more severe disease and changes referral urgency.
Low C3 with normal C4 supports post-infectious disease but is not uniquely diagnostic. C3 should recover within 6–8 weeks; persistent consumption means the working diagnosis must be reopened.
ASO is more often elevated after pharyngitis, whereas anti-DNase B can help after throat or skin infection. A single titre supports preceding exposure but does not prove that every nephritic presentation is post-streptococcal.
Fluid prescription should be written from current outputs and insensible loss, not generic maintenance. The NHSGGC paediatric renal guideline uses urine and other measured losses plus approximately 400 mL/m²/day as a practical insensible estimate.
Volume-mediated hypertension often responds to salt restriction and loop diuresis. Neurological symptoms, severe blood pressure elevation or pulmonary oedema require monitored emergency control; rapid unplanned lowering can impair cerebral and renal perfusion.
Kidney biopsy is unnecessary in a typical improving post-streptococcal course. It becomes relevant with rapidly progressive disease, persistent renal impairment, heavy proteinuria, atypical complement, positive autoimmune studies or diagnostic uncertainty.
Prognosis in children is usually excellent. Persistent microscopic blood alone may last months, but sustained proteinuria, hypertension, impaired eGFR or complement abnormality needs continued nephrology assessment.
Key points
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.
Aetiology
01
Post-streptococcal immunity
Nephritogenic group A streptococcal throat or skin infection precedes inflammatory glomerular immune-complex deposition and complement activation.
02
Other post-infectious disease
Staphylococcal and viral infections can trigger a similar nephritic syndrome, particularly when clinical timing or microbiology differs.
03
Primary glomerulopathy
IgA nephropathy, C3 glomerulopathy and membranoproliferative patterns can present acutely and closely mimic post-infectious glomerular inflammation.
04
Systemic immune disease
Lupus, ANCA vasculitis, anti-GBM disease and IgA vasculitis cause nephritis with additional systemic or serological clues.
Pathophysiology
1
Glomerular immune injury
Immune complexes and complement recruit inflammatory cells that damage glomerular capillary walls and reduce available filtration surface.
2
Glomerular haematuria
Red cells cross damaged filtration barriers, become dysmorphic and may form diagnostic cellular casts within renal tubules.
3
Salt and water retention
Falling filtration and tubular sodium conservation expand extracellular volume, driving oedema, hypertension and potentially severe pulmonary congestion.
4
Complement consumption
Alternative-pathway activation lowers serum C3 transiently in typical post-infectious disease before expected recovery over several weeks.
Clinical features and red flags
Nephritic cluster
Combine cola-coloured urine, oedema, oliguria, hypertension and proteinuria rather than interpreting haematuria alone.
Streptococcal interval
Establish infection type and latency: roughly 1–2 weeks after throat disease or 3–6 weeks after skin infection.
Fluid-overload severity
Assess weight gain, respiratory distress, crackles, gallop rhythm, oedema, urine output and exact fluid intake.
Hypertensive effects
Ask about headache, vomiting, visual change, confusion or seizure and use an age-appropriate blood-pressure cuff.
Systemic clues
Search skin, joints, abdomen, lungs, hearing and family history for vasculitis, lupus or inherited disease.
Atypical trajectory
Track complement, creatinine and proteinuria; persistence or rapid worsening is diagnostically more important than one initial result.
Red flags requiring action
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.
Investigations
01First-line: urinalysis, microscopy and protein:creatinine ratioFirst stepFirst line
Why
Confirm glomerular blood, quantify protein and exclude urinary infection.
Interpretation and limitations
Dysmorphic red cells or red-cell casts support glomerular bleeding; nephrotic-range protein increases severity and referral urgency.
02Renal profile and blood gas
Why
Assess filtration, potassium, bicarbonate and dialysis-threatening complications.
Interpretation and limitations
Trend creatinine and urine output; urgent action follows hyperkalaemia, severe acidosis or rapidly worsening function rather than diagnosis alone.
03Complement C3 and C4
Why
Characterise complement consumption and test the post-infectious trajectory.
Interpretation and limitations
Low C3 with normal C4 supports post-infectious disease; repeat at 6–8 weeks and investigate if C3 remains low.
04ASO and anti-DNase B titres
Why
Seek evidence of recent group A streptococcal infection.
Interpretation and limitations
Interpret with infection site and latency; a raised titre supports exposure but does not replace the complete phenotype.
05Autoimmune tests and kidney biopsy
Differential diagnosis
01
IgA nephropathy
Visible haematuria occurs within a few days of respiratory infection, complement is usually normal and episodes may recur.
02
IgA vasculitis
Palpable lower-limb purpura, abdominal pain and arthralgia accompany haematuria or proteinuria with usually preserved serum complement levels.
03
Lupus nephritis
Low C3 and C4, positive ANA and double-stranded DNA antibodies, cytopenias or systemic features support lupus.
04
Haemolytic uraemic syndrome
Anaemia with fragmentation, thrombocytopenia and AKI after diarrhoea indicates systemic thrombotic microangiopathy rather than isolated nephritis.
05
Alport spectrum disease
Persistent familial haematuria, sensorineural hearing loss and ocular abnormalities indicate an inherited type IV collagen disorder.
Management
01InitialStabilise and phenotype nephritisFirst stepA child has haematuria with oedema, hypertension or reduced urine.+
1Measure paediatric-centile blood pressure, weight, respiratory and neurological status and establish strict fluid balance.
2Obtain urine sediment and protein quantification, renal profile, FBC, albumin, complement and streptococcal evidence.
3Admit when hypertension, oedema, AKI, oliguria, electrolyte disturbance or diagnostic uncertainty requires monitored treatment.
02FluidMatch input to outputSalt and water retention causes oedema or hypertension.+
1Restrict salt and prescribe fluid from measured urine and other losses plus age-appropriate insensible loss.
2Use furosemide for clinical overload under observation and monitor weight, pressure, electrolytes and urine response.
Complications
01
Hypertensive encephalopathy
Severe pressure elevation can cause headache, vomiting, visual disturbance, confusion, seizure and posterior reversible encephalopathy syndrome.
02
Pulmonary oedema
Salt and water retention can overwhelm cardiac and respiratory reserve, producing clinically significant hypoxaemia and acute breathlessness.
03
Acute kidney injury
Marked inflammatory filtration loss can cause oliguria, hyperkalaemia, acidosis and severe uraemic symptoms requiring temporary dialysis support.
04
Rapidly progressive nephritis
Crescentic glomerular injury can destroy renal function quickly and requires urgent biopsy and specialist disease-specific immunosuppression.
05
Persistent renal abnormality
Ongoing hypertension, proteinuria or reduced filtration may signal an alternative glomerulopathy or residual chronic kidney damage.
Monitoring and follow-up
In hospital, record daily weight, accurate input and output, frequent blood pressure and daily urinalysis or protein quantification according to severity.
Trend creatinine, potassium, bicarbonate and sodium more frequently when urine output falls or diuresis begins.
Repeat clinical respiratory and neurological assessment with every important blood-pressure or fluid change.
Confirm C3 recovery at 6–8 weeks when initially low; persistent reduction is not the expected post-streptococcal course.
Continue community blood pressure and proteinuria review after discharge until the renal trajectory is clearly resolving.
Microscopic haematuria alone may persist for 1–2 years, but recurrence or accompanying protein and hypertension changes its significance.
Special situations
Timing separates two diagnoses
Post-streptococcal haematuria follows a latent interval, whereas IgA nephropathy often coincides with the respiratory illness.
Complement is a trajectory
Low C3 initially supports the diagnosis; normalisation by 6–8 weeks is the stronger confirmatory pattern.
Penicillin clears residual streptococcus but established immune-complex glomerular inflammation resolves on its own timescale.
Microscopic blood resolves slowly
Persistent blood alone can be benign during recovery, while persistent protein, pressure or dysfunction is more concerning.
Common pitfalls
01
Do not treat cola-coloured urine as a lower UTI without checking blood pressure, protein and renal function.
02
Do not give routine maintenance fluid to an oliguric overloaded child.
03
Do not use a normal throat culture to exclude a preceding streptococcal trigger.
04
Do not assume raised ASO proves that every nephritic feature is post-streptococcal.
05
Do not forget anti-DNase B when the antecedent infection was cutaneous.
06
Do not omit repeat C3 when it was initially low.
07
Do not chase isolated microscopic haematuria with repeated emergency testing when all higher-risk markers resolve.
08
Do not delay nephrology discussion for hyperkalaemia, rapid creatinine rise or uncontrolled hypertension.
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.
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.
Why
Identify lupus, vasculitis, anti-GBM or alternative pathology when severe or atypical.
Interpretation and limitations
Positive serology, persistent complement abnormality, nephrotic protein, rapid function loss or non-recovery prompts urgent nephrology-led biopsy consideration.
3Add specialist antihypertensive treatment if pressure remains elevated; treat pulmonary oedema or encephalopathy as an emergency.
03StreptococcusEradicate residual infectionPost-streptococcal glomerulonephritis is the supported diagnosis.+
1Obtain throat or skin microbiology when active infection is present and check allergy history.
2Give a complete 10-day penicillin course according to age and current BNFC or local guidance.
3Explain that antibiotics eradicate streptococcus and reduce spread but do not shorten established immune-mediated renal inflammation.
04Follow-upProve expected recoveryThe child's acute renal physiology has stabilised.+
1Follow blood pressure, weight, urine protein, haematuria, creatinine and electrolytes until improving.
2Repeat C3 at 6–8 weeks if initially low and reopen the diagnosis if it has not normalised.
3Refer ongoing proteinuria, hypertension, impaired function, recurrent nephritis or other atypical features for nephrology assessment.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Reduces salt and water overload and often improves volume-mediated hypertension.
Furosemide
For nephritic fluid overload under paediatric supervision, start 0.5 mg/kg orally or intravenously once daily; titrate according to response up to 1 mg/kg per dose twice daily as described in the NHSGGC renal guideline.
Confirm true overload, urine output and perfusion before dosing. Monitor weight, blood pressure, sodium, potassium, creatinine and ototoxicity risk; do not escalate ineffective diuresis instead of arranging dialysis assessment.
Eradicates nephritogenic streptococcus and limits transmission but does not reverse established nephritis.
Phenoxymethylpenicillin
For residual group A streptococcal eradication, give orally for 10 days: age 1 to 5 years 125 mg four times daily, age 6 to 11 years 250 mg four times daily, and age 12 to 17 years 500 mg four times daily, checking current BNFC guidance.
Check immediate penicillin allergy, age, formulation and swallowing. Use a current alternative regimen if genuinely allergic and complete the course; do not represent antibiotic therapy as renal immunomodulation.