Synopsis
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.
- 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.
- 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.
Key red flags
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.
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.
Investigation priorities
Detect and quantify glomerular protein loss and establish a baseline for remission.
Management branches
A child has oedema, heavy proteinuria and hypoalbuminaemia.
- Admit or urgently discuss with paediatrics according to oedema, volume state, renal function and complication risk.
- Confirm protein loss, albumin, renal profile, blood pressure and atypical features; investigate secondary disease selectively.
- Start the specialist prednisolone induction course, salt advice and daily urine monitoring with a written plan.