Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Nephrotic syndrome
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Shock, sepsis or thrombosis
A child with nephrotic syndrome can be visibly oedematous yet intravascularly depleted. Severe abdominal pain, fever, peritonism, breathing difficulty, unilateral limb swelling, neurological deficit, hypotension or poor perfusion indicates infection, thrombosis, pulmonary oedema or hypovolaemia.
Action: Admit urgently, involve paediatric nephrology, obtain cultures and targeted coagulation or imaging without delaying treatment, and assess intravascular volume carefully. Give sepsis therapy, albumin, diuretic, anticoagulation or respiratory support only through a senior paediatric pathway because the wrong fluid or diuretic strategy can worsen shock or overload.
Overview
Recognise nephrotic oedema, confirm heavy protein loss and hypoalbuminaemia, distinguish a typical steroid-sensitive presentation from secondary disease, and manage steroids, volume state, infection and thrombosis risk safely.
The syndrome combines oedema, marked proteinuria and low serum albumin. Hyperlipidaemia results from increased hepatic lipoprotein production and reduced clearance but is not required to recognise an acute child presentation.
Minimal-change nephrotic syndrome is the commonest childhood form. Podocyte and slit-diaphragm dysfunction increases albumin permeability without the inflammatory urine pattern typical of nephritis; light microscopy may be near normal.
Albumin loss lowers plasma oncotic pressure and favours movement of water into interstitial tissues. Effective circulating volume varies: some children are underfilled, whereas others retain sodium primarily and remain intravascularly replete or overloaded.
The clinical consequence is that oedema does not tell the clinician which fluid treatment is safe. Assess pulse, capillary refill, blood pressure, temperature, urine output, abdominal symptoms, recent diuretics and change in weight before intervention.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Oedema with abdominal pain
A child with nephrotic syndrome has tense oedema, tachycardia, cool peripheries, abdominal pain and falling urine output. What is the safest interpretation?
Sources and review status4 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.
History should cover onset, urine froth, infection, medications, atopy, haematuria, rash, joint or abdominal symptoms, family renal disease, thrombosis, immunisation and exposure to varicella or measles.
Examine distribution and severity of oedema, ascites, respiratory status, skin integrity, perfusion and blood pressure. Fever, peritoneal signs, limb asymmetry or neurological abnormality demands complication assessment.
Urine protein:creatinine ratio quantifies protein loss without a 24-hour collection. Microscopy checks for an active sediment; serum albumin, urea, creatinine and electrolytes establish severity and renal safety.
Complement, antinuclear antibodies, infection serology, genetics or biopsy are not routine in every typical first episode. They become important with atypical phenotype, congenital onset, steroid resistance or secondary disease suspicion.
Prednisolone induces remission in most typical childhood cases. Accurate body-surface-area calculation, a defined daily then alternate-day schedule and written stop plan prevent both undertreatment and unplanned prolonged exposure.
Steroids create appetite change, weight gain, mood and sleep disturbance, hypertension, infection susceptibility, bone effects, cataract and adrenal suppression risk. Record cumulative exposure and minimise additional courses through specialist relapse strategy.
Relapse often follows viral illness. Frequent relapsing or steroid-dependent disease may need levamisole, mycophenolate, calcineurin inhibitors, cyclophosphamide or rituximab under specialist protocols; these are not interchangeable primary-care options.
Long-term outcome is generally good in steroid-sensitive disease, but families require practical dipstick teaching, emergency infection advice and a named renal contact. Steroid resistance carries greater risk of focal segmental glomerulosclerosis and chronic kidney disease.
Key points
Nephrotic syndrome is heavy glomerular protein loss causing hypoalbuminaemia and oedema, usually with hyperlipidaemia; urine protein is the quickest diagnostic clue.
Typical childhood presentation is morning periorbital puffiness progressing to dependent, genital or generalised oedema, weight gain, ascites and reduced urine output.
First-line tests are urine dipstick and early-morning protein:creatinine ratio, serum albumin, creatinine and electrolytes, blood pressure, weight and assessment of intravascular volume.
Minimal-change disease causes most typical cases and usually responds to corticosteroids. Atypical age, haematuria, hypertension, low complement, AKI or systemic disease needs broader evaluation.
First episode treatment should be led by paediatrics or nephrology. A common UK regimen is prednisolone 60 mg/m² once daily, maximum 80 mg, for 4 weeks then 40 mg/m² on alternate days, maximum 60 mg, for 4 weeks.
Define remission by urine protein becoming negative or trace on 3 consecutive days; teach daily first-morning dipstick testing and record weight during oedema or intercurrent illness.
Relapse is commonly 3+ or 4+ protein for 3 consecutive days. Restart steroids only according to the child's written renal plan and confirm whether oedema or infection changes disposition.
Aetiology
01
Minimal-change disease
Immune-mediated podocyte dysfunction causes most typical childhood steroid-sensitive cases without substantial glomerular inflammation on routine microscopy.
02
Focal segmental sclerosis
FSGS may be immune, genetic or secondary and is more strongly associated with steroid resistance and progressive kidney disease.
03
Genetic podocytopathy
Congenital, infantile, familial or treatment-resistant disease may result from pathogenic variants affecting essential glomerular filtration-barrier proteins.
04
Secondary systemic disease
Lupus, infection, vasculitis, medicines and other systemic disorders can produce nephrotic protein loss with additional clinical abnormalities.
Pathophysiology
1
Filtration-barrier failure
Podocyte and slit-diaphragm dysfunction allows albumin and other circulating plasma proteins to pass excessively into the urine.
2
Reduced oncotic pressure
Hypoalbuminaemia favours fluid movement into interstitial tissues, producing clinically visible periorbital, dependent, genital and peritoneal oedema.
3
Sodium retention
Renal sodium conservation and intrarenal retention expand extracellular fluid, with variable effective circulating volume between children.
4
Protein-loss consequences
Loss of immunoglobulins and anticoagulant proteins contributes to infection and thrombosis, while hepatic lipoprotein production causes hyperlipidaemia.
Clinical features and red flags
Oedema pattern
Look for morning periorbital swelling, dependent or genital oedema, ascites, rapid weight gain and reduced urine output.
Urinary protein loss
Marked dipstick protein and a high early-morning protein:creatinine ratio support glomerular protein leakage.
Volume phenotype
Integrate pulse, perfusion, blood pressure, abdominal pain, urine output and recent diuretic exposure before giving fluid or diuresis.
Fever, peritonism, limb asymmetry, chest symptoms or neurological change can signal infection or thrombosis.
Steroid burden
Record current and cumulative dose, relapse pattern, growth, mood, sleep, blood pressure, glucose risk and infection exposure.
Red flags requiring action
Poor perfusion, tachycardia, abdominal pain, low urine output or rising creatinine may indicate intravascular depletion despite generalised oedema.
Fever, peritonism or unexplained deterioration suggests spontaneous bacterial peritonitis, cellulitis, pneumonia or sepsis and requires urgent cultures and antibiotics.
Sudden breathlessness, pleuritic pain, unilateral leg swelling, severe headache, seizure or focal deficit raises concern for venous thrombosis.
Investigations
01First-line: urine dipstick and protein:creatinine ratioFirst stepFirst line
Why
Detect and quantify glomerular protein loss and establish a baseline for remission.
Interpretation and limitations
Heavy proteinuria with oedema and hypoalbuminaemia supports nephrotic syndrome; blood or leucocytes require sediment and differential review.
02Serum albumin, renal profile and lipids
Why
Confirm hypoalbuminaemia and assess kidney function, electrolytes and metabolic consequences.
Interpretation and limitations
AKI or major electrolyte abnormality changes fluid safety and suggests complicated or atypical disease.
03Urine microscopy and culture
Why
Identify an active sediment and exclude infection when symptoms or steroid treatment make it relevant.
2Use salt restriction and disease treatment for uncomplicated oedema; avoid routine aggressive diuresis.
Complications
01
Serious bacterial infection
Spontaneous peritonitis, cellulitis, pneumonia and sepsis occur through immune-protein loss, oedematous tissue and immunosuppressive treatment exposure.
02
Venous thrombosis
Loss of anticoagulant proteins, haemoconcentration, inflammation and immobility increase deep venous, pulmonary and cerebral thrombosis risk.
03
Hypovolaemic kidney injury
Sepsis, diarrhoea or excessive diuresis can reduce effective renal perfusion despite persistent visible generalised peripheral oedema.
04
Pulmonary oedema
Primary sodium retention, renal impairment or inappropriate albumin and fluid administration can cause acute respiratory compromise in children.
05
Treatment toxicity
Repeated corticosteroids or steroid-sparing agents can cause infection, hypertension, metabolic, growth, bone, ocular and gonadal harm.
Monitoring and follow-up
Measure first-morning urine protein daily during active disease and illness, then at the frequency in the individual renal plan.
Record weight, oedema, intake and urine output; rapid weight change can reveal fluid movement before examination alone.
Check blood pressure at presentation and during corticosteroid or calcineurin-inhibitor treatment.
Trend creatinine, electrolytes and albumin when oedema is severe, urine output falls or fluid treatment is used.
Monitor steroid effects including mood, sleep, appetite, growth, obesity, glucose, infection, bone and eye risk.
Review immunisation status and provide a clear plan for fever and varicella or measles exposure while immunosuppressed.
Track relapse frequency and cumulative steroid exposure to identify frequent relapsing or steroid-dependent disease early.
Special situations
Oedema can conceal depletion
Interstitial fluid excess can coexist with poor circulating volume, so reflex diuresis may precipitate shock and AKI.
Urine dipsticks guide home care
Three consecutive negative or trace mornings define practical remission, while persistent heavy protein identifies relapse early.
Steroid response carries information
Prompt remission supports steroid-sensitive disease; resistance changes prognosis and triggers pathology or genetic assessment.
Abdominal pain has dangerous causes
It may reflect hypovolaemia, spontaneous peritonitis or thrombosis, not merely discomfort from ascites.
Relapse count matters
Frequent relapse and steroid dependence identify children whose treatment toxicity may exceed the benefit of repeated steroid courses.
Common pitfalls
01
Do not diagnose allergy from periorbital oedema without checking urine protein.
02
Do not infer intravascular overload solely from the amount of peripheral oedema.
03
Do not give unsupervised albumin or high-dose diuretic to a potentially underfilled child.
04
Do not ignore fever or abdominal pain in an immunocompromised child with ascites.
05
Do not continue an initial prednisolone course without a documented daily and alternate-day stop plan.
06
Do not label microscopic haematuria alone steroid resistance, but investigate sustained atypical features.
07
Do not use NSAIDs for pain when renal perfusion may be vulnerable.
08
Do not manage recurrent relapse without tracking cumulative steroid toxicity.
Do not give routine rapid diuresis. Salt restriction and treatment of the glomerular disease are foundational; specialist albumin plus furosemide is reserved for selected severe oedema or hypovolaemia.
Infection risk is increased by urinary immunoglobulin loss, oedematous tissue and immunosuppression. Fever or abdominal pain needs urgent assessment, not routine home steroid escalation.
Thrombosis risk rises with haemoconcentration, severe hypoalbuminaemia, immobility, central lines, sepsis and inherited thrombophilia; routine anticoagulation is not universal.
Avoid NSAIDs and intravascularly depleting medicines. Check vaccination and varicella exposure plans before or during immunosuppression and avoid live vaccines when contraindicated.
Failure to remit after the defined steroid course, frequent relapses, steroid dependence or steroid toxicity requires specialist reassessment and possible steroid-sparing therapy.
Hypertension, macroscopic haematuria, low complement, systemic features or significant AKI is atypical for minimal-change steroid-sensitive disease.
Congenital or infantile onset, age above about 12 years, persistent complement abnormality, steroid resistance or family history lowers the threshold for genetic testing or biopsy.
Tense ascites, respiratory compromise, severe genital oedema, inability to mobilise or skin breakdown requires inpatient specialist fluid management.
Reference diagnosis: kidney biopsy or genetics
Why
Define pathology or inherited disease in selected resistant, congenital or atypical cases.
Interpretation and limitations
Not routine before treating a typical first episode; timing is determined by paediatric nephrology and steroid response.
3
For severe oedema, hypovolaemia or respiratory compromise, admit for specialist albumin, diuretic or fluid management with close observations.
03RelapseUse the written renal planUrine is 3+ or 4+ protein on 3 consecutive days or oedema returns.+
1Confirm dipstick technique, symptoms, weight, infection and complication red flags.
2Contact the renal team and restart prednisolone only at the prescribed relapse dose and stop point.
3Document remission after three consecutive negative or trace days and continue alternate-day treatment for the planned duration.
04Atypical responseEscalate steroid resistanceEscalationRemission does not occur within the specialist-defined induction period or atypical features develop.+
1Check adherence, dose calculation, infection and whether the diagnosis remains nephrotic syndrome.
2Refer promptly for genetic, immunological and biopsy consideration rather than extending steroids indefinitely.
3Plan steroid-sparing therapy, thrombosis and infection prevention, and kidney-function surveillance through paediatric nephrology.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Induces remission in typical childhood steroid-sensitive nephrotic syndrome.
Prednisolone for first episode
A common UK paediatric regimen is 60 mg/m² orally once daily, maximum 80 mg, for 4 weeks followed by 40 mg/m² orally on alternate days, maximum 60 mg, for 4 weeks; use the treating renal unit's current protocol.
Calculate body surface area and maximum carefully, give a written stop schedule, screen infection and exposure risk, monitor blood pressure, growth, behaviour and glucose, and never prolong therapy to compensate for steroid resistance without nephrology review.
Restores remission in a confirmed relapse of previously steroid-sensitive disease.
Prednisolone for relapse
Under the child's renal plan, use 60 mg/m² orally once daily, maximum 80 mg, until urine is negative or trace for 3 consecutive days, then 40 mg/m² on alternate days, maximum 60 mg, for 4 weeks.
Confirm the relapse definition, intercurrent infection and complication red flags. Repeated or dependent courses require specialist steroid-sparing review; families should not start treatment without a current written plan.