ReviewKidney research and clinical practice2018
Immune mechanisms in the different phases of acute tubular necrosis.
Review in Kidney research and clinical practice, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- Acute, high dose ethylene glycol administration produces no neuroinflammation, no abnormal brain or liver histology, significant urinary oxalate excretion, and minimal nephrotoxicity in male CD-1 mice.Toxicology reports · 2026Article
- Targeting YAP1-Mediated Tubular Cell Senescence to Attenuate Maladaptive Repair and Fibrotic Transition After Acute Kidney Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The Pathology and Blood Biochemistry of Juvenile Lates calcarifer on Diets Contaminated With Mycotoxins, Histamines and Rancid Fats-A Case Study.Journal of fish diseases · 2025Article
- Pathogenesis and management of renal fibrosis induced by unilateral ureteral obstruction.Kidney research and clinical practice · 2024Article
- IKK1 aggravates ischemia-reperfusion kidney injury by promoting the differentiation of effector T cells.Cellular and molecular life sciences : CMLS · 2023Article
- NETosis: an emerging therapeutic target in renal diseases.Frontiers in immunology · 2023Review
- Deficiency of mindin reduces renal injury after ischemia reperfusion.Molecular medicine (Cambridge, Mass.) · 2022Article
- Role of T cells in ischemic acute kidney injury and repair.The Korean journal of internal medicine · 2022Review
- SAP130 released by damaged tubule drives necroinflammation via miRNA-219c/Mincle signaling in acute kidney injury.Cell death & disease · 2021Article
- Review
- Clusterin regulates macrophage expansion, polarization and phagocytic activity in response to inflammation in the kidneys.Immunology and cell biology · 2021Article
- Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021Review
- Rhabdomyolysis-Induced AKI Was Ameliorated in NLRP3 KO Mice via Alleviation of Mitochondrial Lipid Peroxidation in Renal Tubular Cells.International journal of molecular sciences · 2020Article
- RNA-Seq identifies condition-specific biological signatures of ischemia-reperfusion injury in the human kidney.BMC nephrology · 2020Article
- SerpinB2 Regulates Immune Response in Kidney Injury and Aging.Journal of the American Society of Nephrology : JASN · 2020Article
- Plasma Concentrations of Extracellular DNA in Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury is a clinical syndrome that can be caused by numerous diseases including acute tubular necrosis (ATN). ATN evolves in several phases, all of which are accompanied by different immune mechanisms as an integral component of the disease process. In the early injury phase, regulated necrosis, damage-associated molecular patterns, danger sensing, and neutrophil-driven sterile inflammation enhance each other and contribute to the crescendo of necroinflammation and tissue injury. In the late injury phase, renal dysfunction becomes clinically apparent, and M1 macrophage-driven sterile inflammation contributes to ongoing necroinflammation and renal dysfunction. In the recovery phase, M2-macrophages and anti-inflammatory mediators counteract the inflammatory process, and compensatory remnant nephron and cell hypertrophy promote an early functional recovery of renal function, while some tubules are still badly injured and necrotic material is removed by phagocytes. The resolution of inflammation is required to promote the intrinsic regenerative capacity of tubules to replace at least some of the necrotic cells. Several immune mechanisms support this wound-healing-like re-epithelialization process. Similar to wound healing, this response is associated with mesenchymal healing, with a profound immune cell contribution in terms of collagen production and secretion of profibrotic mediators. These and numerous other factors determine whether, in the chronic phase, persistent loss of nephrons and hyperfunction of remnant nephrons will result in stable renal function or progress to decline of renal function such as progressive chronic kidney disease.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.