Membranous nephropathy !

Membranous nephropathy is an immune kidney disease that causes heavy protein loss in the urine in adults and raises the risk of blood clots.

Updated 2026-11-01

Structures involved

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In the clinical exam

Nephrotic vs nephritic syndrome

Why it happens

What it is

An immune-mediated glomerular disease in which antibodies bind to antigens on the podocyte and form subepithelial deposits, thickening the glomerular basement membrane. It is a classic cause of nephrotic syndrome in adults.

Who gets it

It is one of the commonest causes of nephrotic syndrome in white adults, peaking at 40–60 years and more frequent in men. About 70–80% of cases are primary, most with anti-PLA2R antibodies. Secondary forms linked to hepatitis B, lupus, cancers and drugs must be sought, and hepatitis B and lupus are relevant in Latin America.

Causes

Primary: autoantibodies against podocyte antigens, mostly PLA2R (phospholipase A2 receptor) and less often THSD7A
Infections: hepatitis B (also in children), hepatitis C, syphilis, malaria
Autoimmune disease: systemic lupus erythematosus (lupus class V)
Solid tumours: lung, colon, stomach, breast, prostate
Drugs: NSAIDs, gold, penicillamine, captopril

Risk factors

Age 40–60 years and male sex
Chronic hepatitis B or C
Lupus
Solid cancer, especially in people over 60
Exposure to NSAIDs and certain drugs

Pathophysiology

Antibodies bind to antigens on the podocyte surface (in situ immune complexes) and activate complement, injuring the podocyte. The subepithelial deposits are surrounded by new basement membrane, producing the typical spikes and thickening of the capillary walls. Proteinuria is heavy, and urinary loss of antithrombin plus increased hepatic clotting factors makes this the glomerular disease with the highest risk of renal vein thrombosis.

Classification

Primary (anti-PLA2R or other podocyte antigen) versus secondary
Risk groups by proteinuria, kidney function and antibody level: low, moderate, high and very high risk of progression

Symptoms and signs

Gradual swelling of the legs and ankles, sometimes generalised
Foamy urine
Weight gain from fluid
Fatigue
Sometimes high blood pressure and microscopic haematuria
Some patients have subnephrotic proteinuria found on routine testing

Diagnosis

Clinical: Nephrotic syndrome in a middle-aged adult; history for drugs, infections, lupus and cancer symptoms; age-appropriate cancer screening.
Tests: Urine protein-to-creatinine ratio, albumin, lipids and creatinine; serum anti-PLA2R antibodies (a positive test in typical nephrotic syndrome strongly supports primary disease and can avoid biopsy in selected cases; levels track activity); hepatitis B and C, HIV, syphilis, ANA and complement. Biopsy shows thickened capillary walls, spikes on silver stain, granular IgG and C3 on immunofluorescence and subepithelial deposits on electron microscopy.
Imaging: Kidney ultrasound; Doppler ultrasound or CT/MR venography if renal vein thrombosis is suspected; chest imaging and other studies for cancer when indicated.

Differential diagnosis

Focal segmental glomerulosclerosis
Minimal change disease
Diabetic kidney disease
Amyloidosis
Lupus nephritis class V

Goal of treatment

Reduce proteinuria and achieve remission, prevent thrombosis and protect kidney function, treating any secondary cause directly.

Treatment

Medical: Supportive care for all: ACE inhibitors or ARBs, diuretics, statins and blood pressure control; low-risk patients are observed because about a third remit spontaneously.
Medical: Immunosuppression for moderate to high risk of progression: rituximab, calcineurin inhibitors, or cyclophosphamide alternating with glucocorticoids.
Medical: Prophylactic anticoagulation in selected patients with very low albumin and low bleeding risk; full anticoagulation after a thrombosis.
Lifestyle: Low-salt diet and normal protein intake; treating hepatitis B, cancer or stopping the responsible drug in secondary forms.
Follow-up: Monitoring: weight, oedema, blood pressure, proteinuria, creatinine and anti-PLA2R levels over time; watching for signs of thrombosis and drug adverse effects.

Complications

Renal vein thrombosis, deep vein thrombosis and pulmonary embolism
Progression to chronic kidney disease
Hyperlipidaemia and cardiovascular disease
Infections and adverse effects of immunosuppression

Prognosis

Follows a rule of thirds: about one third remit spontaneously, one third have persistent proteinuria with stable function and one third progress toward kidney failure over years. Falling anti-PLA2R levels predict remission.

Test yourself

Think of the answer, then tap the question to see it.

Which antibody identifies most cases of primary membranous nephropathy?

Anti-phospholipase A2 receptor (anti-PLA2R) antibody.

Which glomerular disease carries the highest risk of renal vein thrombosis?

Membranous nephropathy.

What does silver stain show in membranous nephropathy?

Spikes along the basement membrane around subepithelial deposits.

Which infection is a classic secondary cause of membranous nephropathy, including in children?

Hepatitis B.

Which lupus nephritis class has a membranous pattern?

Class V.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Membranous nephropathy: MedlinePlus Medical Encyclopedia (MedlinePlus (U.S. National Library of Medicine), 2024); Nephrotic Syndrome in Adults (NIDDK (National Institutes of Health), 2024).

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Representative model, for educational purposes only.

Kidneys highlighted on the Durgical 3D model