Publication: Uric acid is a useful tool to predict contrast-induced nephropathy
dc.contributor.coauthor | Mendi, Mehmet Ali | |
dc.contributor.coauthor | Oksuz, Fatih | |
dc.contributor.coauthor | Turak, Osman | |
dc.contributor.coauthor | Yayla, Cagri | |
dc.contributor.coauthor | Ozcan, Firat | |
dc.contributor.coauthor | Afsar, Baris | |
dc.contributor.coauthor | Johnson, Richard J. | |
dc.contributor.department | School of Medicine | |
dc.contributor.kuauthor | Kanbay, Mehmet | |
dc.contributor.schoolcollegeinstitute | SCHOOL OF MEDICINE | |
dc.date.accessioned | 2024-11-09T23:46:13Z | |
dc.date.issued | 2017 | |
dc.description.abstract | Developing contrast-induced nephropathy (CIN) after primary percutaneous coronary intervention (pPCI) has a negative impact on survival and morbidity. We assessed the predictive value of serum uric acid (SUA) for the development of CIN in patients with ST-segment elevation myocardial infarction (STEMI) who underwent pPCI. Contrast-induced nephropathy was defined an increase of 25% or 0.5 mg/dL in creatinine concentrations within 72 hours after pPCI. Patients were divided into 2 groups according to admission median SUA level. Serum uric acid level was <5.4 mg/dL (group 1; n = 222) and 5.4 mg/dL (group 2; n = 228). Compared to group 1, development of CIN (12% vs 20%, P < .001) was significantly greater in group 2. Using a cut point of >5.45 mg/dL, the SUA level predicted development of CIN with a sensitivity of 70% and specificity of 67%. In multiple logistic regression analysis, SUA level, diabetes mellitus, left ventricular ejection fraction <50%, contrast volume, estimated glomerular filtration rate, and C-reactive protein level emerged as independent predictors of CIN. In conclusion, elevated SUA is an independent risk factor for the development of CIN after pPCI in patients with STEMI. | |
dc.description.indexedby | WOS | |
dc.description.indexedby | Scopus | |
dc.description.indexedby | PubMed | |
dc.description.issue | 7 | |
dc.description.openaccess | NO | |
dc.description.publisherscope | International | |
dc.description.sponsoredbyTubitakEu | N/A | |
dc.description.volume | 68 | |
dc.identifier.doi | 10.1177/0003319716639187 | |
dc.identifier.eissn | 1940-1574 | |
dc.identifier.issn | 0003-3197 | |
dc.identifier.quartile | Q3 | |
dc.identifier.scopus | 2-s2.0-85021794142 | |
dc.identifier.uri | https://doi.org/10.1177/0003319716639187 | |
dc.identifier.uri | https://hdl.handle.net/20.500.14288/13935 | |
dc.identifier.wos | 404713900010 | |
dc.keywords | Uric acid | |
dc.keywords | Contrast-induced nephropathy | |
dc.keywords | Myocardial infarction | |
dc.keywords | Primary percutaneous coronary intervention percutaneous coronary interventıon | |
dc.keywords | Chronic kidney-disease | |
dc.keywords | Cardiovascular risk-factors | |
dc.keywords | hyperuricemia | |
dc.keywords | Allopurinol | |
dc.keywords | Injury | |
dc.keywords | Cells | |
dc.keywords | Pathogenesıs | |
dc.keywords | Dysfunction | |
dc.keywords | Mechanism | |
dc.language.iso | eng | |
dc.publisher | Sage | |
dc.relation.ispartof | Angiology | |
dc.subject | Peripheral Vascular Disease | |
dc.title | Uric acid is a useful tool to predict contrast-induced nephropathy | |
dc.type | Journal Article | |
dspace.entity.type | Publication | |
local.contributor.kuauthor | Kanbay, Mehmet | |
local.publication.orgunit1 | SCHOOL OF MEDICINE | |
local.publication.orgunit2 | School of Medicine | |
relation.isOrgUnitOfPublication | d02929e1-2a70-44f0-ae17-7819f587bedd | |
relation.isOrgUnitOfPublication.latestForDiscovery | d02929e1-2a70-44f0-ae17-7819f587bedd | |
relation.isParentOrgUnitOfPublication | 17f2dc8e-6e54-4fa8-b5e0-d6415123a93e | |
relation.isParentOrgUnitOfPublication.latestForDiscovery | 17f2dc8e-6e54-4fa8-b5e0-d6415123a93e |