Posters
AKI: Mechanisms - Inflammation and Repair
October 22, 2026 | 10:00 AM - 12:00 PM
Location: Exhibit Hall A, Convention Center
Session Description
Poster Session
Posters
CD36-Driven Lipid Uptake Creates a Druggable Macrophage Checkpoint in AKI
Endogenous Extracellular Vesicle Engineering Delivers HNF4α mRNA to Attenuate Cisplatin-Induced Acute Kidney and Liver Injury
Ferroptotic Injury Drives Two Distinct Proximal Tubule Cell Fate Trajectories During Maladaptive Kidney Repair
Tubule-Derived CCN1 Drives Renal Repair via αvβ5-STAT6-ARG1-Dependent Reprogramming of Macrophages
Tubular Cell-Derived Enolase 1 Promotes Inflammatory Macrophage Activation and AKI
Loss of Myeloid PD-L1 Attenuates Ischemic AKI Through Modulating Macrophage Metabolic Fitness
Macrophage GPR30 Protects Against AKI Progression by Sustaining Peroxisome Proliferator-Activated Receptor γ (PPARγ)-Dependent Cholesterol Homeostasis
Infusion of Bone Marrow-Derived Macrophages (BMDM) from Normal Mice Protects Mice from Cisplatin (CP)-Induced AKI
Myeloid-Specific Deletion of Smoothened Aggravates AKI
Notch2-Dependent Functions of Renal Mononuclear Phagocytes at Baseline and in AKI
Natural Killer T Cells in Cardiac Surgery-Associated AKI
Mast Cell-γδ T Cell Axis Orchestrates Ultra-Early Kidney Injury via IL-17 Programming
CD8+CD103+ T Cells Mediate Kidney Recovery After Severe AKI
High-Resolution Spatial Transcriptomics During AKI Identifies an Unexpected Kidney Red Blood Cell Transcriptional Response
High-Resolution Spatial Transcriptomics Reveals Candidate Molecular Pathways That Mediate Interactions Between Immune Cells and Renal Tubules During AKI
RGMb Restrains Regulatory T Cell (Treg) Differentiation and Promotes the AKI-to-CKD Transition
Lymphoid Aggregates in Kidney Disease Resolve into Two Transcriptionally Distinct Subtypes That Demarcate Divergent Tubular Injury Microenvironments
Spatial Transcriptomics of Tertiary Lymphoid Tissues (TLTs) and Injured Tubules in Unilateral Ischemia-Reperfusion (uIR) Kidneys
mTOR Inhibition Reduces Tertiary Lymphoid Tissues (TLTs) and Ameliorates AKI-to-CKD Transition in a Unilateral Ischemia-Reperfusion (uIR) Model of Severe AKI
Immunometabolic Molecule CD38 and Experimental AKI
Additive Protective Effects of CD36 Inhibition by Peptide 5A in Combination with Cilastatin Against Vancomycin-Induced Nephrotoxicity
Role of Adenosine Triphosphate (ATP) Leakage-Mediated Metabolic-Immune Activation in AKI-to-CKD Transition
Kidney-Derived Circulating Osteopontin Drives Hippocampal Neuroinflammation and Neurologic Dysfunction in AKI Independent of Uremia but with Age-Dependent Vulnerability
Endogenous Cellular RNA Drives Sterile Kidney Inflammation Through the RIG-I/MAVS Pathway
Cosmetics to Kidneys: Ethyl-Paraben Exposure Induces Inflammatory and Kidney Injury Responses and the Protective Effects of Curcumin and Metformin in an In Vitro Kidney Model
BRCC3 Regulation of TRAF2/NF-κB in Renal Tubular Epithelial Cells: Implications in AKI
Longitudinal Dynamics of Urinary Renal Tubular Epithelial Cells and T Cells Provides Insights into Adaptation After Kidney Injury and Potential Novel Biomarkers
ANXA3 Mediates Pyroptosis of Renal Tubular Epithelial Cells in Septic AKI via the NLRP6 Inflammasome Pathway
Delaying Stress Granule Disassembly by PARG Inhibition Attenuates Renal Tubular Epithelial Cell Pyroptosis in AKI
Inhibition of Integrin αvβ3 Attenuates Ischemia-Reperfusion-Induced AKI-to-CKD Progression
Proximal Tubule-Specific FoxO1 Deletion Ameliorates Kidney Injury by Inhibition of CCL20 Expression
APOL1 G2 Risk Variant Promotes Maladaptive Repair and Inflammation After Ischemia-Reperfusion Injury
Staphylococcus aureus Niches in the Kidney
Development of a New Prophylactic Strategy for AKI by Acquisition of Injury Tolerance
Diabetes Increases Severity of Sepsis-Associated AKI While Preserving a Targetable TLR9 Pathway
Early Glomerular and Tubular Biomarkers of Kidney Injury Reflect Different Aspects of Sepsis Severity in Murine Sepsis
Mechanistic Study of Thrombotic Microangiopathy Induced by Lipopolysaccharide and Inflammatory Cytokines
Myeloid Cell TRPM2 and Uromodulin (Tamm-Horsfall Protein) Mediate Immune Response and Organ Damage in Sepsis
Administration of MARY1, a Novel HTR2B Antagonist, Attenuates Sepsis-Induced AKI in Mice
Cross-Model Proteomics of Acute Tubular Injury in Mouse Kidney Reveals Etiology-Specific Signatures in Sepsis, Nephrotoxicity, and Ischemia-Reperfusion Injury
Age-Related Differences in Renal Endothelial Transcriptome in Sepsis-Associated AKI
Towards Personalized Targeting of Endothelial Barrier Dysfunction in Sepsis-Associated AKI
Identification of Epigenetic Signatures of Maladaptive Repair in the AKI-to-CKD Transition (EpiAKI Study)