Acute Kidney Injury Research

Dynamics of cell states and alternative splicing following kidney ischemia-reperfusion injury

The paper analyzes bulk RNA-seq data from a kidney IRI mouse experiment to identify temporal phases and alternatively spliced genes, revealing potential splicing regulators involved in injury and repair.

SUBCLINICAL ACUTE KIDNEY DISEASE: URINARY PROTEOMIC DIVERGENCE FOLLOWING NEPHROTOXIC AND ISCHAEMIC INJURY

This study identifies urinary proteomic signatures associated with subclinical AKD following nephrotoxic or ischemic injury in rats, revealing persistent structural damage despite functional recovery.

Androgens Drive SOX9 Upregulation in Injured Proximal Tubular Cells

This study shows that SOX9 upregulation in injured proximal tubular cells is driven by androgens in males but blunted in females, revealing sex-specific repair mechanisms in AKI.

Spatial analysis reveals the cellular microenvironments and mechanisms of inflammation and kidney injury in acute interstitial nephritis

The paper identifies the CXCL9-CXCR3 axis and NAMPT as key drivers of inflammation and kidney injury in acute interstitial nephritis using spatial transcriptomics and imaging.

Differentiating Hepatic and Renal Toxicity Reveals CYP-Independent Mechanisms of Acetaminophen-Induced Acute Kidney Injury

This study shows that acetaminophen-induced acute kidney injury occurs through CYP-independent mechanisms, even when hepatic CYP2E1 is deleted, highlighting the need for kidney-specific therapies.

Spatial metabolomics reveals persistent localized niche-specific metabolic failure in kidneys following ischemia-reperfusion injury

The paper uses spatial metabolomics and transcriptomics to identify persistent metabolic failure in kidney niches after ischemia-reperfusion injury, highlighting mitochondrial dysfunction in otherwise healthy areas.

ELMO1 dependent efferocytosis protects from nephrotoxin induced acute kidney injury

This study investigates the role of ELMO1 in acute kidney injury, finding that ELMO1 deficiency increases tissue injury in cisplatin-induced AKI but not in ischemia-reperfusion models.

Endothelial Prolyl Hydroxylase 3 Mitigates Maladaptive Inflammation to Promote Post-Ischemic Kidney Repair

This study identifies endothelial PHD3 as a regulator of kidney repair after ischemia, showing its role in suppressing inflammation and fibrosis through HIF-dependent mechanisms.

Long-chain polyphosphates induce glomerular microthrombi and exacerbate LPS-induced acute kidney injury in mouse

This study shows that long-chain polyphosphates cause kidney damage and worsen LPS-induced acute kidney injury in mice by forming microthrombi and increasing inflammation.

Stiffness sensing fuels matrix-driven metabolic reboot for kidney repair and regeneration

This study identifies Mfap2 as a key ECM component that regulates kidney repair by linking mechanical cues to metabolic reprogramming through Esr2-mediated transcriptional control.

Elucidation of Puberulic Acid-Induced Nephrotoxicity Using Stem Cell-based Kidney Organoids

This study uses kidney organoids to demonstrate that puberulic acid causes nephrotoxicity by inducing mitochondrial dysfunction and oxidative stress.

Y665F variant of mouse Stat5b protects against acute kidney injury through transcriptomic shifts in renal gene expression

The paper investigates the protective role of the Stat5bY665F mutation in acute kidney injury using mouse models and transcriptomic analyses.

Pathophysiological response in experimental trauma-related acute kidney injury

This study develops a murine model of trauma-related acute kidney injury and identifies early renal stress responses and inflammatory changes.

Impact of nephrotoxins and oxidants on survival and transport function of hiPSC-derived renal proximal tubular cells

This study examines how nephrotoxins and oxidants affect the differentiation and function of iPSC-derived renal proximal tubular cells, finding that differentiating cells are highly sensitive to these agents.

Loss of long-chain acyl-CoA dehydrogenase protects against acute kidney injury

This study shows that loss of LCAD protects against acute kidney injury by reducing oxidative stress and enhancing peroxisomal fatty acid oxidation.

Protamine Protects Against Vancomycin Induced Kidney Injury

This study shows protamine delays vancomycin-induced kidney injury in rats by reducing urinary KIM-1 levels, without significantly inhibiting OAT1, OAT3, or OCT2.

Post-ischemic inactivation of HIF prolyl hydroxylases in endothelium promotes maladaptive kidney repair by inducing glycolysis

This study shows that inactivating PHD enzymes in endothelial cells after ischemic kidney injury promotes maladaptive repair through glycolysis and MCT4, which can be reversed by MCT4 inhibitors.

Urinary single-cell sequencing captures intrarenal injury and repair processes in human acute kidney injury

This study uses urinary single-cell RNA sequencing to analyze injury and repair processes in acute kidney injury, identifying distinct cellular and molecular dynamics.

Temporal and sex-dependent gene expression patterns in a renal ischemia-reperfusion injury and recovery pig model

This study identifies sex-dependent gene expression patterns in a pig model of renal ischemia-reperfusion injury, revealing temporal and sexual dimorphism in injury and recovery processes.

Single Cell Profiling of Acute Kidney Injury Reveals Novel Transcriptional Signatures, Mixed Identities and Epithelial-to-Stromal Crosstalk

This study uses single-cell RNA sequencing to identify novel transcriptional signatures and epithelial-stromal interactions in acute kidney injury.

Cell profiling of mouse acute kidney injury reveals conserved cellular responses to injury

The paper uses single nucleus RNA sequencing to identify a proinflammatory and profibrotic proximal tubule cell state in mouse AKI that fails to repair, suggesting it as a therapeutic target.

Prediction of Acute Kidney Injury with a Machine Learning Algorithm using Electronic Health Record Data

This study develops a machine learning model to predict acute kidney injury using electronic health records, achieving higher accuracy than traditional clinical scores.