<p>Autoantibody-driven autoimmune diseases, such as systemic lupus erythematosus, frequently affect organs such as the kidney. The differentiation and function of pathogenic immune cells that drive these diseases are in part controlled by their metabolic programming. For diseases that affect the kidney, the response of kidney cells to immune-mediated injury is also in part controlled by metabolic changes. Immune cells that promote the production of autoantibodies and/or infiltrate the kidney in lupus nephritis are sustained by enhanced glycolysis and mitochondrial oxidation. These metabolic processes are also enhanced in the mesangial and glomerular endothelial cells of patients with lupus nephritis and animal models of lupus nephritis, which may contribute to tissue injury. Similar alterations in metabolic processes might be involved in other autoimmune diseases that affect the kidney, including IgA nephropathy and ANCA-associated vasculitis. Insights into metabolic changes that occur in the context of autoimmune-mediated kidney diseases might have therapeutic implications. Despite the complexity of metabolic alterations presented by specific immune and renal cells in these autoimmune diseases, targeting of glycolysis, mitochondrial oxidation or iron metabolism could offer novel opportunities to enhance existing treatments for autoimmune-mediated kidney injury.</p>