ReviewThe Journal of clinical investigation2025
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.
Review in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed.
- Spatial analysis reveals cellular microenvironments and mechanisms of inflammation and injury in acute interstitial nephritis.Nature communications · 2026Article
- Rewiring the mitochondrial NADMaterials today. Bio · 2026Article
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- Article
- Arginase-1 Expressing Macrophages Interact with Myofibroblasts to Regulate Insulin-Like Growth Factor-1-Dependent Tubule Repair.Kidney360 · 2026Article
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2026Article
- Investigating the roles of macrophage age and circulating extracellular vesicles in cytoprotection of hypoxic renal tubular cell stress.BMC molecular and cell biology · 2026Article
- Article
- Mas-related G protein-coupled receptor type D deficiency promotes tubulointerstitial injury and fibrosis associated with proteinuria in male mice.Physiological reports · 2026Article
- Pathophysiology and Management of Sepsis-associated Acute Kidney Injury.Clinics in chest medicine · 2026Review
- DUSP26 protects against acute kidney injury by dephosphorylating p53 at serine 312.Nature communications · 2026Article
- Therapeutic rewiring of ceRNA networks: a computational pipeline for drug repurposing in acute kidney injury via circRNA-miRNA-mRNA axis disruption.Human genomics · 2026Review
- Mitochondrial dysfunction in sepsis-associated acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Associations between metabolic indices and the prevalence of simple renal cysts among hospitalized patients with hypertension in Xinjiang, China: a large-scale cross-sectional study.Frontiers in cardiovascular medicine · 2026Article
- Article
- Post-translational protein S-palmitoylation in renal tubular injury: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Poor prognosis of acute kidney injury superimposed on chronic kidney disease: potential mechanisms, risk factors and novel biomarkers.Frontiers in molecular biosciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Acute kidney injury (AKI) encompasses pathophysiology ranging from glomerular hypofiltration to tubular cell injury and outflow obstruction. This Review will focus on the tubulointerstitial processes that underlie most cases of AKI. Tubular epithelial cell (TEC) injury can occur via distinct insults, including ischemia, nephrotoxins, sepsis, and primary immune-mediated processes. Following these initial insults, tubular cells can activate survival and repair responses or they can develop mitochondrial dysfunction and metabolic reprogramming, cell-cycle arrest, and programmed cell death. Developing evidence suggests that the fate of individual tubular cells to survive and proliferate or undergo cell death or senescence is frequently determined by a biphasic immune response with initial proinflammatory macrophage, neutrophil, and lymphocyte infiltration exacerbating injury and activating programmed cell death, while alternatively activated macrophages and specific lymphocyte subsets subsequently modulate inflammation and promote repair. Functional recovery requires that this reparative phase supports proteolytic degradation of tubular casts, proliferation of surviving TECs, and restoration of TEC differentiation. Incomplete resolution or persistence of inflammation can lead to failed tubular repair, fibrosis, and chronic kidney disease. Despite extensive research in animal models, translating preclinical findings to therapies remains challenging, emphasizing the need for integrated multiomic approaches to advance AKI understanding and treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.