Synopsis
Recognise membranous nephropathy, separate primary immune disease from secondary causes, and coordinate risk-based supportive and specialist treatment safely.
- Membranous nephropathy is an immune-complex glomerular disease in which subepithelial deposits and podocyte injury produce heavy, often nephrotic-range proteinuria.
- Anti-PLA2R antibodies strongly support primary membranous nephropathy in the right phenotype, but a negative result neither excludes the disease nor removes the need to search for secondary causes.
- Evaluate medicines, malignancy, hepatitis B and C, autoimmune disease and other clinical clues before calling a case primary; biopsy antigen staining may refine this assessment.
Key red flags
Sudden pleuritic pain, hypoxia, unilateral leg swelling or loin pain may indicate pulmonary, deep venous or renal-vein thrombosis.
Investigation priorities
Quantify protein loss and identify blood or an active sediment.
Management branches
An adult has heavy albuminuria with suspected nephrotic syndrome.
- Confirm quantitative proteinuria, serum albumin, renal trajectory and clinical complications while reviewing previous results.
- Request anti-PLA2R and a history-led secondary screen, including prescribed and non-prescribed medicines, infection risks and malignancy symptoms.
Membranous nephropathy is likely or confirmed and the patient is clinically stable.
Key medicines
ACE inhibitor or angiotensin-receptor blockerSelect and titrate one agent using the current CKD formulary, blood pressure, potassium and eGFR; do not combine ACE inhibition with an ARB.
Rituximab in selected primary diseaseUse only through the specialist membranous-nephropathy protocol and current NHS commissioning arrangements; regimen, premedication and retreatment are determined by the renal team.