Posters
AKI: Mechanisms - Metabolism and Repair
October 23, 2026 | 10:00 AM - 12:00 PM
Location: Exhibit Hall A, Convention Center
Session Description
Poster Session
Posters
Metabolic Pathways as Therapeutic Targets in Sepsis-Induced AKI
Single-Nucleus Long-Read RNA Sequencing Unravels Isoform-Level Regulation of Gene Expression in Normal and Acutely Injured Proximal Tubule Cells
Multi-Omic Integration Uncovers Sex-Specific Rewiring of NAD+ Metabolism and Signaling in AKI
Loss of NAD+ Salvage Biosynthesis Modulates Tubular Injury in AKI
Nicotinamide N-Methyltransferase (NNMT)-Dependent Enzymatic Activity Drives SOX9-Associated Maladaptive Proximal Tubular (PT) Repair
Role of Endothelial Lactate Monocarboxylate Transporter (MCT1/4) in AKI Repair
Urinary Branched-Chain Amino Acids (BCAAs) Reflect Proximal Tubular Amino Acid Transport and Metabolic Dysfunction in AKI
Innate Fear Odor Stimulation Reprograms Renal Energy Homeostasis and Protects Against AKI
Melatonin Attenuates Sepsis-Associated AKI by Alleviating Aberrant Metabolic Reprogramming Through SIRT3-Mediated Deacetylation of Hypoxia-Inducible Factor (HIF)-1α
Perifusate Metabolomics of Kidney Tubules Reveals Nutrient-Dependent Modulation of Stress Response
C5aR Deficiency Attenuates Kidney Ischemia-Reperfusion Injury by Enhancing Lipid Metabolism
Metabolic Adaptations in Mitochondria of African Spiny Mice (Acomys cahirinus) Promote Proximal Tubular Cytoresistance to AKI
Fenofibrate Regulates Lipid Biogenesis and Mitochondrial Fatty Acid Flux to Counter Renal Lipotoxic Stress
Inhibition of Npt2a Rescues Proximal Tubular Mitochondrial Function via the Annexin A2-YAP Pathway in AKI
Ablation of p53 Mitigates Cisplatin-Induced Mitochondrial Dysfunction and Kidney Injury
IRE1α Drives Renal Ischemia-Reperfusion Injury by Directly Sensing Adenosine Triphosphate (ATP) Levels and Promoting Mitochondrial Calcium Loading at Endoplasmic Reticulum-Mitochondrial Associated Membranes (ER-MAMs)
Hypothermia Preserves Mitochondrial Oxidative Phosphorylation and Suppresses RNA Processing and Ribosome Biogenesis in Murine Ischemia-Reperfusion Injury (IRI)
Targeted E3 Ubiquitin Ligase MAP3K1-Induced Mitophagy Alleviates AKI
Colistin-Induced AKI Is Driven by Maladaptive TFEB Hyperactivation and Rescued by Ultrasmall Copper Nanoparticles
Exploring AKI as a Cause of Diaphragm Dysfunction in the Intensive Care Unit
Metabolomic Profile of Muscle Wasting in Critically Ill Patients with AKI Receiving CRRT
CREBRF Rewires Proximal Tubular Metabolism in Kidney Injury and Remodeling
Glutamine Treatment Improves Cardiac Energy Metabolism in Mice with AKI
Treatment of AKI by Activation of Branched-Chain Amino Acid (BCAA) Catabolism
Delayed Treatment with Dapagliflozin Highlights a Potential Reversibility of Maladaptive Repair in Late Phases of AKI-to-CKD Transition in Rats
Gut-Kidney Crosstalk in Sepsis-Associated AKI: Gut Microbiota Dysbiosis and the Role of Metabolite Trimethyllysine in Renal Tubular Mitochondrial Dysfunction
Obesity-Driven AKI-to-CKD Transition Is Independent of AMPK-ACC Signaling in Weight-Adjusted, Low-Dose Folic Acid-Induced AKI
Dietary Protein Restriction Mitigates AKI-to-CKD Transition After Ischemia-Reperfusion Injury
Fasting Enhances Ischemic Tolerance Due to Restoration of Adenosine Triphosphate (ATP) Levels via Elevation of β-Oxidation Activity
Pseudostructure Reconstruction of Kidney Nephrons Enables Comparative Three-Dimensional (3D) Analysis of Molecular Gradients
Mobilization of Antioxidant Vitamin Reserves to Combat Oxidative Stress in Cardiorenal Syndrome Due to Right Ventricular Failure
Moderate Physical Training Preserves Renal Hemodynamics and Attenuates Tenofovir-Induced Tubular Injury
Multifactorial Biomarker Pattern of Exercise-Associated AKI in Trail Runners
Tubule-Specific Deletion of Cyclin G1 Attenuates Maladaptive Repair and Tubular Dedifferentiation in a Repeat Low-Dose Cisplatin AKI-to-CKD Model
FANCD2 Regulates the Transition from Adaptive to Maladaptive Repair in the Kidney Through Transcription Factor Coregulatory Networks
Plasma-Derived Fetuin-A Repletion Attenuates Renal Ischemia-Reperfusion Injury and Maladaptive Repair
Highly Senescent Subpopulation of Failed Repair Proximal Tubular Cells Drives Kidney Injury Progression
Dual Bioactive Flavonol-Based Carbonized Quantum Dots Protect Kidneys by Targeting DcR2 to Inhibit Tubular Senescence and Hinder AKI-to-CKD Transition
Targeted Intervention for DcR2 Alleviates AKI by Modulating Tubular Senescence
Renal Proximal Tubular Vgll4 Triggers Maladaptive Repair After AKI
Inhibition of Fatty Acid Metabolism Protects Against AKI