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Nephrology›Condition·Updated Jun 27, 2026·v1

Nephrotic Syndrome

Nephrotic syndrome is a clinical syndrome of massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia caused by podocyte injury. Diagnosis involves confirming proteinuria, serologic testing, and kidney biopsy. Management includes supportive nephroprotection and disease-specific immunosuppression. Prognosis varies by histology, with early proteinuria reduction being key.

High Evidence391 references·10,238 words·41 min read·v1
nephrotic syndromepodocytopathyminimal change diseasefocal segmental glomerulosclerosismembranous nephropathyproteinuriahypoalbuminemiaedemarituximabanti-PLA2RAPOL1KDIGO

Quick Reference

RxDrug of choicePrednisone for MCD/SSNS; Rituximab for MN and steroid-dependent NS
AltAlternativesCalcineurin inhibitors (tacrolimus, cyclosporine), cyclophosphamide, mycophenolate mofetil, obinutuzumab
⊘AvoidNSAIDs, ACEi/ARB in pregnancy, live vaccines on high-dose steroids, non-dihydropyridine CCBs
DxTest of choiceUrine protein-to-creatinine ratio (UPCR) + serum albumin + anti-PLA2R antibody + kidney biopsy
ScKey scoreKDIGO CKD heat-map, anti-PLA2R titer, Toronto risk score for MN, International IgAN Prediction Tool
→When to referNephrology for biopsy and immunosuppression; transplant for ESKD
Nephrotic syndrome requires prompt diagnosis, etiology-specific immunosuppression, and aggressive complication prevention; early proteinuria reduction to <0.5 g/d is the strongest modifiable predictor of kidney survival.
Nephrotic syndrome is a clinical syndrome defined by the tetrad of massive proteinuria (≥3.5 g/24 h in adults), hypoalbuminemia (<3.0 g/dL), edema, and hyperlipidemia. It results from podocyte injury due to autoimmune, circulating factor, or genetic causes. The most common primary glomerulopathies are minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and membranous nephropathy (MN). Diagnosis requires confirmation of nephrotic-range proteinuria, serologic testing (anti-PLA2R antibodies), and often kidney biopsy. Management includes supportive nephroprotection (RAAS blockade, SGLT2 inhibitors) and disease-specific immunosuppression (corticosteroids, rituximab, calcineurin inhibitors). Complications such as thromboembolism, infection, and acute kidney injury require proactive prevention. Prognosis varies by histology, with early proteinuria reduction being the strongest modifiable predictor of kidney survival.

Overview and Recommendations

Background

  • •Nephrotic syndrome affects approximately 2-4 per 100,000 adults annually, with a higher incidence in children (1.15-16.9 per 100,000). It is a leading indication for kidney biopsy, accounting for ~30% of native biopsies. The syndrome carries significant morbidity from edema, infection, and thromboembolism, and untreated 5-year mortality can exceed 50% in certain subtypes.
  • •The three dominant mechanistic axes are autoantibody-mediated podocytopathy (anti-PLA2R in , anti-nephrin in ), circulating permeability factors (primary ), and monogenic podocyte defects (NPHS2, TRPC6, APOL1). All converge on foot-process effacement and slit-diaphragm disruption.
  • •Primary glomerulopathies are classified by histology: (MCD), normal light microscopy with diffuse foot-process effacement; (FSGS), segmental sclerosis with Columbia subtypes; (MN), subepithelial immune deposits with PLA2R antigen in 70-80%; and (MPGN), mesangial proliferation with double contours.
  • •Secondary causes include , lupus nephritis, infections (hepatitis B/C, HIV), drugs (NSAIDs, pamidronate, immune checkpoint inhibitors), and malignancies. The pretest probability is dominated by age, ethnicity, and geography: MCD in young children, FSGS in African Americans (APOL1-driven), and MN in older white adults.
  • •The paradigm shift in management includes the use of anti-CD20 therapy ( ) as first-line for MN and steroid-dependent nephrotic syndrome, and the addition of to RAAS blockade for nephroprotection. Genetic testing is now recommended for steroid-resistant nephrotic syndrome before age 25, identifying a monogenic cause in ~30%.

Evaluation

  • •Suspect nephrotic syndrome in any patient presenting with periorbital or dependent edema, foamy urine, and weight gain over days to weeks. Ask about onset tempo (acute in MCD, insidious in MN/FSGS), preceding infections, drug exposures, family history of kidney disease, and systemic symptoms (rash, arthritis, fever) suggesting secondary causes.
  • •Examine for pitting edema (periorbital, presacral, scrotal/labial), ascites, pleural effusions, and signs of thromboembolism (unilateral leg swelling, dyspnea, flank pain). Blood pressure is often low in the "underfill" state but may be elevated in secondary causes.
  • •Order a first-morning urine protein-to-creatinine ratio (UPCR), a ratio ≥3.0-3.5 g/g confirms nephrotic-range proteinuria. A 24-hour urine collection for protein ≥3.5 g/1.73 m² is the gold standard but not always necessary.
  • •Measure serum albumin (<3.0 g/dL confirms hypoalbuminemia), creatinine/eGFR, and a lipid panel (elevated total cholesterol and triglycerides). Check complement C3/C4, low levels suggest lupus nephritis, infection-related GN, or C3 glomerulopathy.
  • •Order anti-PLA2R antibody testing in all adults with suspected membranous nephropathy. A titer >14 RU/mL has >95% specificity for primary MN and can obviate the need for biopsy in elderly or high-risk patients.
  • •Perform a full serologic panel for secondary causes: ANA, anti-dsDNA, ANCA, anti-GBM, hepatitis B/C, HIV, serum protein electrophoresis with free light chains, and cryoglobulins. Tailor based on clinical context.
  • •Obtain a renal ultrasound to exclude obstruction, assess kidney size, and evaluate for renal vein thrombosis with Doppler (especially in MN with heavy proteinuria).
  • •Indications for kidney biopsy: all adults with nephrotic syndrome except those with a clear secondary cause or positive anti-PLA2R with typical presentation. In children, biopsy is reserved for steroid-resistant nephrotic syndrome (SRNS), frequent relapses on CNI, or atypical features.
  • •Biopsy must be processed for light microscopy, immunofluorescence (IgG, IgA, IgM, C3, C1q, kappa/lambda, PLA2R), and electron microscopy. Key patterns: MCD (normal LM, negative IF, foot-process effacement on EM), FSGS (segmental sclerosis, IgM/C3 in sclerotic segments), MN (thickened GBM, granular IgG, subepithelial deposits).
  • •In FSGS, differentiate primary (diffuse foot-process effacement) from secondary (segmental effacement, adaptive changes) and genetic forms. Consider genetic testing for SRNS in children and selected adults, especially if onset before age 25 or family history.
  • •In MN that is PLA2R-negative, test for THSD7A, NELL1, EXT1/2, and other antigens by mass spectrometry if available. Rule out malignancy (colon, lung, prostate) per guidelines.
  • •Also consider: urine sediment for oval fat bodies and fatty casts; serum albumin <2.0 g/dL increases thromboembolic risk; and in children, assess for congenital nephrotic syndrome if onset in first 3 months.

Management

  • •Initiate supportive nephroprotection in all patients with proteinuria >0.5 g/day: start an ACE inhibitor or ARB (e.g., 10-40 mg daily or 50-100 mg daily), titrated to maximum tolerated dose. Add an SGLT2 inhibitor ( 10 mg daily or 10 mg daily) once eGFR ≥20 mL/min/1.73 m². Target proteinuria <0.5 g/day.
  • •For minimal change disease (MCD) in adults: start 1 mg/kg/day (max 80 mg) for 4-16 weeks. In children: prednisolone 2 mg/kg/day (max 60 mg) for 4-6 weeks, then alternate-day taper. Over 80% achieve remission.
  • •For steroid-dependent or frequently relapsing MCD: add a steroid-sparing agent. First-line is 375 mg/m² (single dose or two doses 2 weeks apart). Alternatives: 0.05-0.1 mg/kg/day (trough 5-10 ng/mL) or 2 mg/kg/day for 8-12 weeks.
  • •For primary focal segmental glomerulosclerosis (FSGS): start prednisone 1 mg/kg/day for 4-16 weeks. If no remission, switch to a calcineurin inhibitor: 3-5 mg/kg/day (trough 100-150 ng/mL) or tacrolimus 0.05-0.1 mg/kg/day (trough 5-10 ng/mL). Rituximab has limited evidence but may be tried in CNI-resistant cases.
  • •For membranous nephropathy (MN): first-line therapy is 1 g IV on days 1 and 15. If rituximab is contraindicated or ineffective, use cyclical
    • corticosteroids (STARMEN protocol: alternating monthly cycles of cyclophosphamide 2.5 mg/kg/day PO for 3 months and prednisone). Alternative: tacrolimus for up to 12 months.
  • •For IgA nephropathy with nephrotic-range proteinuria: optimize RAAS blockade and SGLT2 inhibition. If proteinuria remains >0.75 g/d despite maximal supportive care, consider corticosteroids ( 0.8 mg/kg/day, taper) or targeted-release budesonide 9 mg daily for 9 months.
  • •In steroid-resistant nephrotic syndrome (SRNS): perform genetic testing before escalating immunosuppression. Patients with monogenic causes (NPHS1, NPHS2, WT1, TRPC6) do not benefit from immunosuppression; manage with supportive care and early transplant evaluation.
  • •Anti-thrombotic prophylaxis: consider prophylactic anticoagulation in adults with membranous nephropathy and serum albumin <2.5 g/dL. Use 40 mg SC daily or (target INR 2-3). DOACs have lower bleeding risk but higher thrombotic events; use with caution.
  • •Manage edema with sodium restriction (<2 g/day) and loop diuretics ( 20-80 mg daily, titrated to urine output). For diuretic resistance, add a thiazide ( 2.5-5 mg daily) or consider ultrafiltration.
  • •Monitor for complications: check serum potassium, creatinine, and albumin monthly during induction. For patients on CNIs, monitor trough levels every 3 months. For rituximab, check CD19 count and IgG levels; consider IVIG if IgG <400 mg/dL and recurrent infections.
  • •Vaccinate against pneumococcus (PCV20 or PPSV23), influenza annually, and COVID-19. Live vaccines (MMR, varicella) are safe during moderate corticosteroid therapy (<2 mg/kg/day or <20 mg/day prednisone).
  • •What NOT to do: avoid NSAIDs in all nephrotic patients due to risk of AKI and sodium retention. Do not use albumin routinely for diuresis. Do not start finerenone in non-diabetic nephrotic syndrome. Avoid non-dihydropyridine CCBs (diltiazem, verapamil) as they worsen proteinuria.
  • •When to refer: refer to nephrology for kidney biopsy, initiation of immunosuppression, and management of complications. Refer for transplant evaluation when eGFR <30 mL/min/1.73 m² or within 1 year of expected dialysis start.
  • •For post-transplant recurrence of FSGS: start plasmapheresis (1.5 plasma volume exchanges, 3-5 sessions/week) and high-dose cyclosporine. Add rituximab 375 mg/m² weekly ×4 if refractory.
  • •Discharge criteria for hospitalized patients: stable fluid balance with oral diuretics, no acute complications (thromboembolism, infection, AKI), and clear follow-up plan with nephrology within 1-2 weeks.

Board Review — High Yield

  • •Minimal change disease, most common cause in children, steroid-sensitive, diffuse foot-process effacement on EM.
  • •Anti-PLA2R antibodies, present in 70% of membranous nephropathy; titer correlates with disease activity and guides therapy.
  • •APOL1 risk variants, increase risk of FSGS and HIV-associated nephropathy in African Americans; odds ratio 5-10.
  • •Rituximab, first-line for membranous nephropathy and steroid-dependent nephrotic syndrome; reduces relapse rate by 73% (NNT=2).
  • •Thromboembolism, highest risk in membranous nephropathy with albumin <2.5 g/dL; consider prophylactic anticoagulation.
  • •Genetic testing, indicated in steroid-resistant nephrotic syndrome before age 25; 30% have monogenic cause (NPHS2, WT1, TRPC6).
  • •KDIGO proteinuria target, <0.5 g/d for IgA nephropathy; <1.5 g/g for FSGS.
  • •Congenital nephrotic syndrome, Finnish type due to NPHS1 mutation; presents in first 3 months; requires early nephrectomy and dialysis.

Deep Dive — Evidence Details

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