ArticleKidney international2014
The urea decomposition product cyanate promotes endothelial dysfunction.
Article in Kidney international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Impact of Uremic Toxins on Endothelial Dysfunction in Chronic Kidney Disease: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Review
- The Physiological Roles and Pathological Implications of Urea Transporters in the Cardiovascular System.Biomedicines · 2025Review
- High-density lipoproteins. Part 2. Impact of disease states on functionality.American journal of preventive cardiology · 2025Article
- Isocyanic acid-mediated NLRP3 carbamoylation reduces NLRP3-NEK7 interaction and limits inflammasome activation.Science advances · 2025Article
- Association Between Blood Urea Nitrogen and Delirium in Critically Ill Elderly Patients Without Kidney Diseases: A Retrospective Study and Mendelian Randomization Analysis.CNS neuroscience & therapeutics · 2025Article
- Protein carbamylation in atherosclerotic plaques correlates with uremia and disease progression, localizing predominantly to foam cells.Frontiers in immunology · 2025Article
- Review
- HDL and chronic kidney disease.Atherosclerosis plus · 2023Article
- Endothelial Cell Dysfunction and Increased Cardiovascular Risk in Patients With Chronic Kidney Disease.Circulation research · 2023Review
- Halogenation Activity of Mammalian Heme Peroxidases.Antioxidants (Basel, Switzerland) · 2022Review
- Heme Peroxidases at Unperturbed and Inflamed Mucous Surfaces.Antioxidants (Basel, Switzerland) · 2021Review
- Arterial Remodelling in Chronic Kidney Disease: Impact of Uraemic Toxins and New Pharmacological Approaches.Journal of clinical medicine · 2021Review
- Article
- Enhanced neutrophil apoptosis accompanying myeloperoxidase release during hemodialysis.Scientific reports · 2020Article
- Very Low Protein Diet for Patients with Chronic Kidney Disease: Recent Insights.Journal of clinical medicine · 2019Review
- Microbiota issue in CKD: how promising are gut-targeted approaches?Journal of nephrology · 2019Review
- Protein Carbamylation: A Marker Reflecting Increased Age-Related Cell Oxidation.International journal of molecular sciences · 2018Article
- Biochemical and Clinical Impact of Organic Uremic Retention Solutes: A Comprehensive Update.Toxins · 2018Review
- Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
The dramatic cardiovascular mortality of patients with chronic kidney disease is attributable in a significant proportion to endothelial dysfunction. Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear. Immunohistochemical analysis performed in the present study revealed that carbamylated epitopes associate mainly with endothelial cells in human atherosclerotic lesions. Cyanate treatment of human coronary artery endothelial cells reduced expression of endothelial nitric oxide synthase, and increased tissue factor and plasminogen activator inhibitor-1 expression. In mice, administration of cyanate, promoting protein carbamylation at levels observed in uremic patients, attenuated arterial vasorelaxation of aortic rings in response to acetylcholine without affecting the sodium nitroprusside-induced relaxation. Total endothelial nitric oxide synthase and nitric oxide production were significantly reduced in aortic tissue of cyanate-treated mice. This coincided with a marked increase of tissue factor and plasminogen activator inhibitor-1 protein levels in aortas of cyanate-treated mice. Thus, cyanate compromises endothelial functionality in vitro and in vivo. This may contribute to the dramatic cardiovascular risk of patients suffering from chronic kidney disease.
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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.