Membranous nephropathy (MN) is a primary glomerular disease commonly causing adult nephrotic syndrome. Characterized by thickened glomerular capillary walls due to immune complex deposition, MN is a complex autoimmune disorder. Its pathogenesis involves immune deposit formation, complement activation, and a heightened risk of renal failure. Central to MN is immune system dysfunction, particularly the dysregulation of B and T cell responses. B cells contribute to renal injury through the production of autoantibodies, particularly IgG targeting the phospholipase A2 receptor (PLA2R) on podocytes, while T cells modulate immune responses that influence disease progression. Metabolic reprogramming alters lymphocyte survival, differentiation, proliferation, and function, potentially triggering autoimmune processes. Although the link between immune cell metabolism and MN remains underexplored, this review highlights recent advances in understanding immune metabolism and its role in MN. These insights may provide novel biomarkers and therapeutic strategies for MN treatment.