## Diagnosis: Membranous Nephropathy **Key Point:** Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in adults, accounting for 30–40% of cases in developed countries and 10–20% in Asia. ### Histological Features | Feature | Membranous Nephropathy | | --- | --- | | Light microscopy | Diffuse thickening of GBM; normal cellularity | | Electron microscopy | **Spike and dome** appearance (subepithelial immune deposits with GBM projections) | | Immunofluorescence | Granular IgG and C3 deposits along capillary wall | | Stage | Stage I–IV (based on EM appearance) | ### Pathogenesis 1. **Primary (idiopathic)** — 75% of cases; autoantibodies to phospholipase A2 receptor (PLA2R) or thrombospondin type-1 domain-containing 7A (THSD7A) 2. **Secondary** — 25% of cases; associated with malignancy (lung, gastric, colon cancer), infections (HBV, HCV, syphilis), autoimmune disease (SLE, rheumatoid arthritis), or drugs (NSAIDs, penicillamine) ### Clinical Presentation **High-Yield:** MN typically presents with: - Nephrotic-range proteinuria (>3.5 g/day) - Preserved renal function initially (unlike FSGS) - Hematuria in 30–50% of cases - Hypertension in 50% of cases - Risk of thromboembolism (hypercoagulability from loss of anticoagulant proteins) ### Management **Clinical Pearl:** Spontaneous remission occurs in 20–30% of patients; therefore, observation is acceptable in low-risk patients. High-risk patients (persistent proteinuria >4 g/day, declining GFR, or serum creatinine >1.3 mg/dL) require immunosuppressive therapy (corticosteroids ± cyclophosphamide or calcineurin inhibitors). **Mnemonic: SPIKE AND DOME** — **S**ubepithelial deposits, **P**rojections of GBM, **I**mmune complexes, **K**idney biopsy finding, **E** (electron microscopy) — characteristic of **M**embranous **N**ephropathy.
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