ReviewJournal of the American Society of Nephrology : JASN2015
Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression.
Review in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 416 papers, 1 of them a synthesis that pooled it.
What it found
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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
416 citing papers in PubMed, 1 synthesis or guideline pooled it, 737 citations in OpenAlex.
- The role of urinary Dickkopf-3 in the prediction of acute kidney injury: a systematic review meta-analysis.International urology and nephrology · 2023Pooled it
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury.Renal failure · 2026Article
- S14G-humanin attenuates renal ischaemia-reperfusion injury, potentially through activation of STAT3 and ERK1/2 signalling pathways in rats.Experimental physiology · 2026Article
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- A novel Keap1-Nrf2 inhibitor 6K delays the progression of AKI-to-CKD by mitigating maladaptive repair.Redox biology · 2026Article
- Modelling ischaemic AKI in human kidney organoids reveals injury-associated epithelial states and macrophage-epithelial crosstalk.Genome medicine · 2026Article
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- Kidney‑enriched lipid nanoparticles delivering ANXA2 alleviate renal ischemia-reperfusion injury via CHMP2A-mediated necroptosis inhibition.Journal of nanobiotechnology · 2026Article
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- Diarylpropionitrile, a selective agonist of estrogen receptor β, protects the kidney against ischemia-reperfusion injury and enhances the repair of tubular epithelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ablation of the renal tubular gluconeogenic enzyme PCK1 drives AKI-to-CKD transition by negatively regulating the TGF-β/Smad3 signaling pathway.Cellular and molecular life sciences : CMLS · 2026Article
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- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- M2 Macrophage membrane-mediated biomimetic nanoparticles carrying ADAM9 siRNA alleviate renal inflammation and fibrosis via the AKT/NF-κB pathway.Journal of nanobiotechnology · 2026Article
- The Aging Kidney and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Integrating clinical, laboratory and quantitative CT features for predicting split renal function in urinary tract obstruction.BMC medical imaging · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Mas-related G protein-coupled receptor type D deficiency promotes tubulointerstitial injury and fibrosis associated with proteinuria in male mice.Physiological reports · 2026Article
- Selenoprotein GPX3 regulates NADPH oxidase expression by inhibiting the MAPK signaling pathway and thereby attenuating the inflammatory response in renal ischemia-reperfusion injury.Genes & diseases · 2026Article
356 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
The transition of AKI to CKD has major clinical significance. As reviewed here, recent studies show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic signaling along multiple pathways. Paracrine products derived therefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast transformation, proliferation, and fibrosis as well as capillary disintegration and rarefaction. Although signals from injured endothelium and inflammatory/immune cells also contribute, tubule injury alone is sufficient to produce the interstitial pathology required for fibrosis. Localized hypoxia produced by microvascular pathology may also prevent tubule recovery. However, fibrosis is not intrinsically progressive, and microvascular pathology develops strictly around damaged tubules; thus, additional deterioration of kidney structure after the transition of AKI to CKD requires new acute injury or other mechanisms of progression. Indeed, experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression. Continued investigation of these pathologic mechanisms should reveal options for preventing renal disease progression after AKI.
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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 OpenQuestion graph.