ArticleAmerican journal of physiology. Renal physiology2018
Divergent effects of AKI to CKD models on inflammation and fibrosis.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- The Predictive Value of Urinary Kidney Injury Molecular 1 for the Diagnosis of Contrast-Induced Acute Kidney Injury after Cardiac Catheterization: A Meta-Analysis.Journal of interventional cardiology · 2020Pooled it
- Renal glucose metabolic enzyme expression during AKI-to-CKD transition.International urology and nephrology · 2026Article
- Inhaled Halogen-Induced Oxidative Renal Damage and Dysfunction: A Lung Heart Kidney Axis.Comprehensive Physiology · 2026Article
- Advancing mesenchymal stem cell therapy for kidney diseases in companion animals: from mechanisms to clinical application.Frontiers in veterinary science · 2026Review
- The Clinical View of Sepsis-Associated AKI: How Basic Science Can Help Solve This Problem.Seminars in nephrology · 2025Review
- Progression of Kidney Fibrosis after Sepsis: Underestimated Role of Resident Macrophages and Recruited Monocytes.Journal of the American Society of Nephrology : JASN · 2025Review
- Bioprinted mesenchymal stem cell microfiber-derived extracellular vesicles alleviate unilateral renal ischemia-reperfusion injury and fibrosis by inhibiting tubular epithelial cells ferroptosis.Bioactive materials · 2024Article
- Podocyte cell-specificPhysiological genomics · 2024Article
- Expanding landscape of coronary microvascular disease in co-morbid conditions: Metabolic disease and beyond.Journal of molecular and cellular cardiology · 2024Review
- TRPC6 Knockout Alleviates Renal Fibrosis through PI3K/AKT/GSK3B Pathway.Current medical science · 2024Article
- Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024Review
- Reciprocal regulation between the molecular clock and kidney injury.Life science alliance · 2023Article
- T CellAntioxidants & redox signaling · 2023Article
- Fibroblast Growth Factor 2 Is Produced By Renal Tubular Cells to Act as a Paracrine Factor in Maladaptive Kidney Repair After Cisplatin Nephrotoxicity.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- Lung cancer-kidney cross talk induces kidney injury, interstitial fibrosis, and enhances cisplatin-induced nephrotoxicity.American journal of physiology. Renal physiology · 2023Article
- The STAT1/HMGB1/NF-κB pathway in chronic inflammation and kidney injury after cisplatin exposure.Theranostics · 2023Article
- Prognostic Nutritional Index Combined with Triglyceride-Glucose Index to Contrast a Nomogram for Predicting Contrast-Induced Kidney Injury in Type 2 Diabetes Mellitus Patients with Acute Coronary Syndrome After Percutaneous Coronary Intervention.Clinical interventions in aging · 2023Article
- The macrocyclic lactone oxacyclododecindione reduces fibrosis progression.Frontiers in pharmacology · 2023Article
- Long-Term Effects of Severe Burns on the Kidneys: Research Advances and Potential Therapeutic Approaches.Journal of inflammation research · 2023Review
- Pifithrin-α ameliorates glycerol induced rhabdomyolysis and acute kidney injury by reducing p53 activation.Renal failure · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Chronic kidney disease (CKD) is a condition with significant morbidity and mortality that affects 15% of adults in the United States. One cause of CKD is acute kidney injury (AKI), which commonly occurs secondary to sepsis, ischemic events, and drug-induced nephrotoxicity. Unilateral ischemia-reperfusion injury (UIRI) without contralateral nephrectomy (CLN) and repeated low-dose cisplatin (RLDC) models of AKI to CKD demonstrate responses characteristic of the transition; however, previous studies have not effectively compared the pathogenesis. We demonstrate both models instigate renal dysfunction, inflammatory cytokine responses, and fibrosis. However, the models exhibit differences in urinary excretory function, inflammatory cell infiltration, and degree of fibrotic response. UIRI without CLN demonstrated worsening perfusion and function, measured with
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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.