<p>Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults and is characterized by subepithelial immune deposits driven by autoantibodies, most commonly anti-PLA2R, with subsequent complement activation and C5b-9–mediated podocyte injury. Emerging evidence suggests that this immune-mediated process is closely intertwined with disturbances in lipid homeostasis. In this review, we propose an immunometabolic framework for MN that highlights the reciprocal interactions between lipid dysregulation and immune activation. Three interrelated mechanistic domains are emphasized. First, cholesterol-enriched lipid rafts on podocyte membranes may facilitate autoantibody binding and immune complex organization, thereby influencing complement activation. Second, systemic dyslipidemia, which is highly prevalent in MN, is associated with increased generation of oxidized low-density lipoprotein (oxLDL), a lipid species that can amplify complement activity and glomerular inflammation. Third, intracellular lipid accumulation and impaired ABCA1-mediated cholesterol efflux may contribute to metabolic reprogramming of adaptive immune cells, including T follicular helper cells, supporting sustained autoantibody production. Clinically, dyslipidemia correlates with proteinuria severity and adverse renal and cardiovascular outcomes, and lipid-lowering therapies have been associated with modest reductions in proteinuria in selected studies. Collectively, these observations support the concept that immune and metabolic pathways are functionally interconnected in MN. Future studies integrating longitudinal multi-omics profiling and computational approaches may help refine patient stratification and guide the development of combined immunologic and metabolic therapeutic strategies.</p><p><?noindent??><b>Clinical trials</b> Not applicable.</p>