ReviewThe Journal of membrane biology2013
Role of contrast media on oxidative stress, Ca(2+) signaling and apoptosis in kidney.
Review in The Journal of membrane biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 58 citations in OpenAlex.
- Indirect bilirubin mitigates tubular vacuolization and injury in experimental contrast nephropathy.BMC nephrology · 2026Article
- Beneficial Effects of Butyrate on Kidney Disease.Nutrients · 2025Review
- Evaluation of hafnium oxide nanoparticles imaging characteristics as a contrast agent in X-ray computed tomography.Radiological physics and technology · 2024Article
- Amlodipine alleviates renal ischemia/reperfusion injury in rats through Nrf2/Sestrin2/PGC-1α/TFAM Pathway.BMC pharmacology & toxicology · 2023Article
- Interleukin-18 and Gelsolin Are Associated with Acute Kidney Disease after Cardiac Catheterization.Biomolecules · 2023Article
- Anti-Apoptotic and Antioxidant Effects of 3-Biomolecules · 2020Article
- Protective effect of cabergoline on mitochondrial oxidative stress-induced apoptosis is mediated by modulations of TRPM2 in neutrophils of patients with endometriosis.Journal of bioenergetics and biomembranes · 2020Article
- Porcine Circovirus Type 2 Induces ORF3-Independent Mitochondrial Apoptosis via PERK Activation and Elevation of Cytosolic Calcium.Journal of virology · 2019Article
- Klotho ameliorates hydrogen peroxide-induced oxidative injury in TCMK-1 cells.International urology and nephrology · 2018Article
- An evaluation of the antioxidant properties of iodinated radiographic contrast media: AnToxicology reports · 2018Article
- A new update for radiocontrast-induced nephropathy aggravated with glycerol in rats: the protective potential of epigallocatechin-3-gallate.Renal failure · 2017Article
- Contrast-induced acute kidney injury: A review of practical points.World journal of nephrology · 2017 · on this mapReview
- NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis.Scientific reports · 2016Article
- Contrast-induced nephropathy in CT: incidence, risk factors and strategies for prevention.European radiology · 2016Review
- Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway.Oxidative medicine and cellular longevity · 2016Article
- A novel approach to contrast-induced nephrotoxicity: the melatonergic agent agomelatine.The British journal of radiology · 2016Article
- Oxidative stress: dual pathway induction in cardiorenal syndrome type 1 pathogenesis.Oxidative medicine and cellular longevity · 2015Article
- Recent reports of Wi-Fi and mobile phone-induced radiation on oxidative stress and reproductive signaling pathways in females and males.The Journal of membrane biology · 2013Review
- Radiographic contrast-media-induced acute kidney injury: pathophysiology and prophylactic strategies.ISRN radiology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contrast media (CM)-induced nephropathy is a common cause of iatrogenic acute renal failure. The aim of the present review was to discuss the mechanisms and risk factors of CM, to summarize the controlled studies evaluating measures for prevention and to conclude with evidence-based strategies for prevention. A review of the relevant literature and results from recent clinical studies as well as critical analyses of published systematic reviews used MEDLINE and the Science Citation Index. The cytotoxicity induced by CM leads to apoptosis and death of endothelial and tubular cells and may be initiated by cell membrane damage together with reactive oxygen species (ROS) and inflammation. Cell damage may be aggravated by factors such as tissue hypoxia, properties of individual CM such as ionic strength, high osmolarity and/or viscosity. Clinical studies indeed support this possibility, suggesting a protective effect of ROS scavenging with the administration of N-acetylcysteine, ascorbic acid erdosteine, glutathione and bicarbonate infusion. The interaction between extracellular Ca(2+), which plays a central role in intercellular contacts and production of ROS, and the in vitro toxicity of CM was also reviewed. The current review addresses the role of oxidative stress in the pathogenesis of CM in the kidney as well as current and potential novel treatment modalities for the prevention of neutrophil activation and CM-induced kidney degeneration in patients. ROS production through CM-induced renal hypoxia may exert direct tubular and vascular endothelial injury. Preventive strategies via antioxidant supplementation include inhibition of ROS generation or scavenging.
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