Membranous nephropathy is the most common cause of nephrotic syndrome in non-diabetic adults, characterized by immune complex deposition on the outer (subepithelial) surface of the glomerular basement membrane. In primary membranous nephropathy, autoantibodies (anti-PLA2R antibodies in 70-80% of cases) target phospholipase A2 receptor on podocyte foot processes, forming in situ immune complexes that activate complement via the membrane attack complex (C5b-9), causing podocyte injury without inflammatory cell infiltration. The damaged podocytes lose their foot process architecture (effacement), disrupting the glomerular filtration barrier and allowing massive protein loss. Clinical presentation is nephrotic syndrome: proteinuria greater than 3.5 g/day, hypoalbuminemia, hyperlipidemia, and peripheral edema. A significant complication is renal vein thrombosis (due to loss of antithrombin III in urine and hypercoagulable state). The nurse monitors daily weights and edema, measures 24-hour urine protein or spot protein-creatinine ratio, monitors serum albumin and lipid levels, assesses for deep vein thrombosis and pulmonary embolism, administers prescribed immunosuppressive therapy (rituximab, calcineurin inhibitors, or cyclophosphamide for high-risk patients), manages sodium restriction and diuretic therapy, monitors anti-PLA2R antibody levels as disease activity markers, and educates about the variable...