Related Experiment Video

Updated: Jul 8, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Metabolic determinants of autoimmune kidney diseases

Yogesh Scindia1, Laurence Morel2

  • 1Department of Medicine, University of Florida, Gainesville, FL, USA.

Nature Reviews. Nephrology
|July 6, 2026
PubMed

Insights

Metabolic changes in immune and kidney cells fuel autoimmune kidney diseases like lupus nephritis. Targeting these metabolic pathways, including glycolysis and mitochondrial oxidation, may offer new therapeutic strategies for kidney injury.

Area of Science:

  • Immunology
  • Nephrology
  • Metabolic Biology

Background:

  • Autoimmune diseases, including systemic lupus erythematosus, often impact the kidney.
  • Immune cell function and kidney cell responses to injury are influenced by metabolic reprogramming.
  • Lupus nephritis involves autoantibody production and immune cell infiltration in the kidney.

Purpose of the Study:

  • To investigate the role of metabolic programming in immune and kidney cells in autoimmune kidney diseases.
  • To explore potential therapeutic targets based on metabolic alterations in lupus nephritis and related conditions.

Main Methods:

  • Analysis of metabolic pathways, including glycolysis and mitochondrial oxidation, in immune cells and kidney cells (mesangial and glomerular endothelial cells).
  • Examination of metabolic alterations in patients with lupus nephritis and relevant animal models.
  • Consideration of metabolic changes in other autoimmune kidney diseases like IgA nephropathy and ANCA-associated vasculitis.

Main Results:

  • Immune cells driving lupus nephritis exhibit enhanced glycolysis and mitochondrial oxidation.
  • Kidney cells (mesangial and glomerular endothelial cells) in lupus nephritis also show heightened metabolic activity, potentially contributing to tissue damage.
  • Similar metabolic alterations may be present in other autoimmune kidney diseases.

Conclusions:

  • Metabolic reprogramming plays a crucial role in the pathogenesis of autoimmune kidney diseases.
  • Targeting metabolic pathways such as glycolysis, mitochondrial oxidation, and iron metabolism presents promising therapeutic avenues for autoimmune-mediated kidney injury.

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