ReviewThe Journal of pharmacology and experimental therapeutics2019
Contrast Induced Acute Kidney Injury and Direct Cytotoxicity of Iodinated Radiocontrast Media on Renal Proximal Tubule Cells.
Review in The Journal of pharmacology and experimental therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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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.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Contrast Media in Hospitalized Patients with Acute Kidney Injury: Renal and Clinical Outcomes.American journal of nephrology · 2026Article
- Experimental study of intravoxel incoherent motion diffusion imaging combined with ultrasound renal resistance index in contrast-induced nephropathy.BMC nephrology · 2025Article
- Human serum albumin-based KBiFJournal of nanobiotechnology · 2025Article
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- Combination drug therapy prevents CIAKI by suppressing ER stress-induced apoptosis.Scientific reports · 2024Article
- The Protective Role of Intermedin in Contrast-Induced Acute Kidney Injury: Enhancing Peritubular Capillary Endothelial Cell Adhesion and Integrity Through the cAMP/Rac1 Pathway.International journal of molecular sciences · 2024Article
- Unveiling the Mysteries of Contrast-Induced Acute Kidney Injury: New Horizons in Pathogenesis and Prevention.Toxics · 2024Review
- Contrast-induced acute kidney injury: a review of definition, pathogenesis, risk factors, prevention and treatment.BMC nephrology · 2024Review
- The intellectual base and global trends in contrast-induced acute kidney injury: a bibliometric analysis.Renal failure · 2023Article
- Atorvastatin reduces contrast media-induced pyroptosis of renal tubular epithelial cells by inhibiting the TLR4/MyD88/NF-κB signaling pathway.BMC nephrology · 2023Article
- The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy.Diagnostics (Basel, Switzerland) · 2022Review
- Protective effect of glycyrrhizin, a direct HMGB1 inhibitor, on post-contrast acute kidney injury.Scientific reports · 2021Article
- Major signaling pathways and key mediators of macrophages in acute kidney injury (Review).Molecular medicine reports · 2021Review
- Gadolinium-Based Contrast Media Nephrotoxicity in Kidney Impairment: The Physio-Pathological Conditions for the Perfect Murder.Journal of clinical medicine · 2021Review
- Anti-Apoptotic and Antioxidant Effects of 3-Biomolecules · 2020Article
- Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence.Oxidative medicine and cellular longevity · 2020Article
- Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The administration of intravenous iodinated radiocontrast media (RCM) to visualize internal structures during diagnostic procedures has increased exponentially since their first use in 1928. A serious side effect of RCM exposure is contrast-induced acute kidney injury (CI-AKI), which is defined as an abrupt and prolonged decline in renal function occurring 48-72 hours after injection. Multiple attempts have been made to decrease the toxicity of RCM by altering ionic strength and osmolarity, yet there is little evidence to substantiate that a specific RCM is superior in avoiding CI-AKI. RCM-associated kidney dysfunction is largely attributed to alterations in renal hemodynamics, specifically renal vasoconstriction; however, numerous studies indicate direct cytotoxicity as a source of epithelial damage. Exposure of in vitro renal proximal tubule cells to RCM has been shown to affect proximal tubule epithelium in the following manner: 1) changes to cellular morphology in the form of vacuolization; 2) increased production of reactive oxygen species, resulting in oxidative stress; 3) mitochondrial dysfunction, resulting in decreased efficiency of the electron transport chain and ATP production; 4) perturbation of the protein folding capacity of the endoplasmic reticulum (ER) (activating the unfolded protein response and inducing ER stress); and 5) decreased activity of cell survival kinases. The present review focuses on the direct cytotoxicity of RCM on proximal tubule cells in the absence of in vivo complications, such as alterations in renal hemodynamics or cytokine influence.
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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.