Membranous nephropathy (MN) is an immune-mediated glomerular disease and the most common cause of nephrotic syndrome in adults. Classical mechanisms involve the binding of autoantibodies, such as anti-PLA2R and anti-THSD7A, to podocytes, causing subepithelial immune deposits, complement activation, and podocyte damage. Lipid metabolism in podocytes is a key regulator of MN pathophysiology, as podocyte cleft diaphragms reside in cholesterol-enriched lipid rafts. Disorders of lipid metabolism, such as excessive uptake or impaired efflux of cholesterol and fatty acids, lead to lipotoxicity with mitochondrial oxidative stress, cytoskeletal reorganization, proinflammatory signaling, podocyte hypertrophy, detachment, and apoptosis. The article examines the interaction of dysregulated lipid profiles with immune damage that exacerbates glomerular damage through inflammation or altered antigen presentation. Biomarkers associated with lipids, such as serum lipids, lipidomic profiles or cholesterol-regulating genes, are related to disease activity. Potential therapies include statins, PCSK9 inhibitors, cyclodextrins, and nuclear receptor agonists to target the metabolic portion of MN. The “lipid-podocyte axis” links podocyte lipid metabolism to the immune pathogenesis of MN.