TextbookRenal MedicineNephrotic Syndrome

Nephrotic Syndrome

Clinical syndrome characterised by heavy proteinuria (>3.5 g/day or uPCR >350 mg/mmol), hypoalbuminaemia (<25 g/L), peripheral oedema, and hyperlipidaemia. In children, minimal change disease is the most common cause; in adults, membranous nephropathy and FSGS predominate.

Key Facts

Nephrotic syndrome is defined by: proteinuria >3.5g/day, hypoalbuminaemia <25g/L, oedema, and hyperlipidaemia Most common cause in children: minimal change disease (80%); in adults: membranous nephropathy (Caucasian) or FSGS (Afro-Caribbean) Key complications: thromboembolism (loss of antithrombin III), infection (loss of immunoglobulins), hyperlipidaemia, AKI Renal vein thrombosis most commonly associated with membranous nephropathy In children: treat empirically with prednisolone without biopsy if typical presentation (age 1-12, no haematuria, normal complement, normal renal function) Adults: renal biopsy is required for all cases to determine underlying cause Thromboprophylaxis with LMWH or warfarin if albumin <20 g/L or significant additional risk factors

Overview

Key Facts

Nephrotic syndrome results from increased glomerular permeability to protein, predominantly albumin. The underlying cause determines treatment and prognosis.

Epidemiology

  • Childhood incidence: 2-7 per 100,000 children/year
  • Adult incidence: 3 per 100,000/year
  • Males more commonly affected in childhood; equal in adults

Aetiology

Children: MCD (80%), FSGS (10%), membranous (5%), MPGN (5%) Adults: Membranous (25-30%), FSGS (20-25%), MCD (10-15%), MPGN (5-10%), diabetic (25%), amyloid (5%) Secondary causes: diabetes, SLE, amyloidosis, drugs (NSAIDs, gold), infections (HBV, HCV, HIV), malignancy

Pathophysiology

  • Glomerular basement membrane damage → loss of charge-selective and size-selective barriers
  • Massive albumin loss in urine → hypoalbuminaemia → reduced oncotic pressure → oedema (underfill hypothesis)
  • In many patients, primary sodium retention by nephrons also contributes (overfill hypothesis)
  • Hepatic response to hypoalbuminaemia: increased lipoprotein synthesis → hyperlipidaemia
  • Loss of antithrombin III, protein C/S, increased fibrinogen → prothrombotic state
  • Loss of immunoglobulins (especially IgG) → increased infection susceptibility

Clinical Presentation

Classic Features

  • Generalised oedema: periorbital (morning), peripheral (dependent), ascites, pleural effusions
  • Frothy urine: due to heavy proteinuria
  • Weight gain: fluid retention

Complications

  • Thromboembolism: DVT, PE, renal vein thrombosis (5-8%)
    • Most common with membranous nephropathy
    • Suspect RVT: sudden flank pain, worsening proteinuria, haematuria
  • Infection: spontaneous bacterial peritonitis (children), cellulitis, pneumonia
    • Encapsulated organisms (pneumococcus) particularly dangerous
  • Hyperlipidaemia: raised total cholesterol, LDL, triglycerides
  • AKI: hypovolaemia, sepsis, bilateral renal vein thrombosis

Red Flags

  • Rapidly declining renal function → exclude RPGN or bilateral RVT
  • Haematuria with nephrotic syndrome → consider FSGS, MPGN, lupus (not typical MCD)
  • Low complement → SLE, MPGN, post-infectious GN
  • Adult >60 with nephrotic syndrome → malignancy screening (especially membranous)

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Nephritic syndromeHaematuria, oliguria, hypertension, modest proteinuriaUrine microscopy, immunology
Heart failureRaised JVP, S3, BNP elevatedBNP, echocardiogram
Liver cirrhosisAscites, spider naevi, low albumin from hepatic failureLFTs, liver USS
Protein-losing enteropathyDiarrhoea, oedema, low albuminFaecal alpha-1 antitrypsin
KwashiorkorMalnutrition, oedema, depigmented hairNutritional assessment

Diagnosis / Investigation

Bedside

  • Urinalysis: 3-4+ protein, assess for blood
  • Blood pressure: may be normal or elevated
  • Daily weight: monitor fluid status
  • Fluid balance: strict input/output

Bloods

  • Urine PCR or 24h urine protein: >350 mg/mmol or >3.5 g/day
  • Serum albumin: <25 g/L
  • Lipid profile: raised cholesterol, triglycerides
  • U&Es: renal function
  • FBC: haemoconcentration (raised Hb/Hct)
  • Immunoglobulins: low IgG
  • C3/C4: low in MPGN, lupus; normal in MCD, FSGS, membranous
  • ANA, dsDNA: lupus screen
  • Anti-PLA2R: membranous nephropathy
  • HbA1c: diabetes
  • Hepatitis B/C, HIV: infection screen
  • Serum/urine electrophoresis: myeloma/amyloid

Imaging

  • Renal USS: kidney size, exclude other pathology
  • Chest X-ray: pleural effusions
  • Renal Doppler: if renal vein thrombosis suspected

Special Tests

  • Renal biopsy: mandatory in adults; not routine in typical childhood nephrotic syndrome

Management

Non-pharmacological

  • Sodium restriction (<2g/day) and fluid restriction if oedematous
  • Dietary protein: adequate but not high-protein diet
  • Leg elevation, compression stockings
  • Pneumococcal vaccination (loss of IgG)

Pharmacological

Oedema management:

  • Loop diuretics: furosemide 40-120mg PO/IV
  • Spironolactone 25-100mg as adjunct
  • IV albumin 20% (100mL) + IV furosemide: for severe/resistant oedema

Thromboprophylaxis:

  • Prophylactic LMWH or warfarin if albumin <20 g/L
  • Full anticoagulation if documented VTE

Hyperlipidaemia:

  • Statins (atorvastatin 20-80mg): for persistent hyperlipidaemia

Specific treatment:

  • Directed by underlying cause (see individual conditions)
  • Children: empirical prednisolone for presumed MCD
  • Adults: guided by biopsy result

Supportive:

  • ACEi/ARB: reduce proteinuria
  • Infection prophylaxis: consider prophylactic penicillin V in children

Referral Criteria

  • All adults → nephrology for biopsy
  • Children not responding to 4 weeks of steroids → paediatric nephrology
  • Complications (VTE, AKI, severe infection) → urgent admission

Prognosis

  • Depends entirely on underlying cause
  • MCD in children: 90-95% remission with steroids; excellent long-term prognosis
  • Membranous nephropathy: rule of thirds (remission/stable/progressive)
  • FSGS: 50-70% progress to ESRD if untreated
  • Diabetic nephropathy: leading cause of ESRD
  • Thromboembolic events: major cause of morbidity/mortality in acute phase
  • Infection: leading cause of mortality in childhood nephrotic syndrome

Other Relevant Information

Nephrotic vs Nephritic Syndrome

FeatureNephroticNephritic
Proteinuria>3.5 g/day<3.5 g/day
HaematuriaUsually absentPresent (with casts)
OedemaSevere, generalisedMild-moderate
Blood pressureNormal or lowElevated
Serum albumin<25 g/LNear normal
Renal functionUsually preservedOften impaired
ComplementUsually normalOften low

Causes by Age Group

Age GroupMost Common Cause
Children (1-12)Minimal change disease
Adolescents/Young adultsFSGS
Adults (30-50)Membranous/FSGS
Elderly (>60)Membranous/amyloid/diabetic