ArticleAmerican journal of physiology. Renal physiology2018
Subclinical kidney injury induced by repeated cisplatin administration results in progressive chronic kidney disease.
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 46 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
46 citing papers in PubMed, 73 citations in OpenAlex.
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Construction of an activatable ratiometric fluorescent nanoprobe for HClO detection and imaging in acute kidney injury models.RSC advances · 2026Article
- Fluvoxamine and lycopene alleviate cisplatin-induced kidney fibrosis by modulating miR-21 and fibrotic signaling pathways.Scientific reports · 2026Article
- Beneficial Effects of Sodium-Glucose Cotransporter 2 Inhibitors in Cisplatin Nephrotoxicity: A Mechanistic Review.Kidney360 · 2026Review
- Indole-3-propionic acid exacerbates cisplatin-induced chronic kidney disease through the AHR/NF-κB signaling pathway.iScience · 2025Article
- Krüppel-Like Factor 6 Induces RNA Polymerase II Subunit RPB1 to Promote Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- TGF-β1 induces ROS to activate ferroptosis via the ERK1/2-WISP1 pathway to promote the progression of renal tubular epithelial cell fibrosis.Cytotechnology · 2025Article
- Oxidative stress and NRF2 signaling in kidney injury.Toxicological research · 2025Review
- A comparative review of murine models of repeated low-dose cisplatin-induced chronic kidney disease.Lab animal · 2025Review
- Remote organ cancer induces kidney injury, inflammation, and fibrosis and adversely alters renal function.American journal of physiology. Renal physiology · 2025Article
- Bardoxolone methyl improves survival and reduces clinical measures of kidney injury in tumor-bearing mice treated with cisplatin.AAPS open · 2025Article
- Adenine-induced animal model of chronic kidney disease: current applications and future perspectives.Renal failure · 2024Review
- Understanding Cisplatin Pharmacokinetics and Toxicodynamics to Predict and Prevent Kidney Injury.The Journal of pharmacology and experimental therapeutics · 2024Review
- Experimental models for preclinical research in kidney disease.Zoological research · 2024Review
- Polyamine Catabolism and Its Role in Renal Injury and Fibrosis in Mice Subjected to Repeated Low-Dose Cisplatin Treatment.Biomedicines · 2024Article
- Decoupling FcRn and tumor contributions to elevated immune checkpoint inhibitor clearance in cancer cachexia.Pharmacological research · 2024Article
- MicroRNA-mediated attenuation of branched-chain amino acid catabolism promotes ferroptosis in chronic kidney disease.Nature communications · 2023Article
- Caught in the crossfire: cancer, cisplatin therapy, and kidney injury.American journal of physiology. Renal physiology · 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
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 2 institutions in 1 country.
Funding
Abstract
Cisplatin is used to treat many solid cancers, but its dose-limiting side effect is nephrotoxicity, causing acute kidney injury in 30% of patients. Previously, we have developed a mouse model that better recapitulates the cisplatin dosing regimen humans receive and found that repeated dosing of cisplatin induces interstitial renal fibrosis. Chronic kidney disease is progressive and is characterized by chronic inflammation, worsening interstitial fibrosis, development of glomerulosclerosis, and endothelial dysfunction. To determine if damage caused by repeated cisplatin dosing results in bona fide chronic kidney disease, mice were treated with our repeated dosing regimen and then aged for 6 mo. These mice had progressive, chronic inflammation and worsened interstitial fibrosis compared with mice euthanized after day 24. Mice aged for 6 mo developed glomerular pathologies, and endothelial dysfunction was persistent. Mice treated with only two doses of cisplatin had little inflammation or kidney damage. Thus repeated dosing of cisplatin causes long-term effects that are characteristic of chronic kidney disease. This translational mouse model of cisplatin injury may better represent the 70% of patients that do not develop clinical acute kidney injury and can be used to identify both biomarkers for early injury, as well as novel therapeutic targets for the prevention of cisplatin-induced 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.