Basic/Clinical Science Session
Metabolic Reprogramming in Diabetic Kidney Disease: From Fuel Selection to Ferroptosis, Including the Barry M. Brenner, MD, Endowed Lectureship
October 22, 2026 | 02:00 PM - 04:00 PM
Location: Room 205, Convention Center
Session Description
Metabolic dysfunction in diabetic kidney disease (DKD) extends beyond hyperglycemia to encompass profound rewiring of cellular fuel use and stress responses. This session explores how tubular epithelial cells shift from fatty acid oxidation toward glycolysis, lactate accumulation, and altered amino acid metabolism, creating vulnerability to regulated cell death pathways, such as ferroptosis. Emphasis is placed on spatial and compartment-specific metabolic programs.
ASN gratefully acknowledges Monarch Pharmaceuticals for support of the Brenner Endowed Lectureship.
Learning Objective(s)
- Identify key metabolic shifts in tubular epithelial cells that drive injury and progression in DKD
- Explain how spatial and compartment-specific metabolic programs influence disease mechanisms and therapeutic targeting
- Describe the role of branched-chain amino acid metabolism and lactate signaling in tubular stress and ferroptosis
Learning Pathway(s)
- Cardiovascular-Kidney-Metabolic (CKM) Health
Moderators
Presentations
- Metabolic Rewiring of Tubular Cells in DKD: The Shift from Fatty-Acid Oxidation to Glycolysis
02:00 PM - 02:30 PM
- Complex Metabolic Reprogramming in Kidney Tubule Cells
02:30 PM - 03:00 PM
- Branched-Chain Amino Acid Metabolism as a Driver of Tubular Stress and Ferroptosis
03:00 PM - 03:30 PM
- Targeting Metabolic Vulnerabilities in DKD and Therapeutic Strategies: The Barry M. Brenner, MD, Endowed Lectureship
03:30 PM - 04:00 PM