Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/35021
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dc.contributor.authorMert, Mehmet-
dc.contributor.authorDursun, Belda-
dc.contributor.authorYağcı, Ahmet Baki-
dc.contributor.authorÇetin Kardeşler, Ayşen-
dc.contributor.authorŞenol, Hande-
dc.contributor.authorDemir, Süleyman-
dc.date.accessioned2020-06-10T08:58:41Z
dc.date.available2020-06-10T08:58:41Z
dc.date.issued2020-
dc.identifier.issn1573-2584-
dc.identifier.issn0301-1623-
dc.identifier.urihttps://hdl.handle.net/11499/35021-
dc.identifier.urihttps://doi.org/10.1007/s11255-019-02336-6-
dc.description.abstractINTRODUCTION AND PURPOSE: Arterial stiffness is an independent predictor of cardiovascular disease in chronic kidney disease (CKD). Cardio-ankle vascular index (CAVI) is a newly developed method used to assess arterial stiffness, independent of changes in blood pressure. CAVI reflects stiffness and atherosclerosis at the thoracic, abdominal, common iliac, femoral, and tibial artery levels. In predialysis stage 3-5 diabetic and nondiabetic CKD patients, CAVI levels and its relation to atherosclerosis-associated risk factors including monocyte-chemoattractant protein-1 (MCP-1), sclerostin, fibroblast growth factor-23 (FGF-23), Klotho, and 25-OH vitamin D were determined. MATERIALS AND METHODS: The study was performed on three age-matched and gender-matched groups. Group 1 included 46 stage 3-5 nondiabetic CKD patients, group 2 included 44 stage 3-5 diabetic CKD patients, and group 3 included 44 non-uremic controls. All subjects underwent CAVI measurement. Serum glycated hemoglobin (HbA1c), total calcium, phosphorus, parathormone, FGF-23, Klotho, MCP-1, sclerostin, and 25-OH vitamin D were determined using standard methods. RESULTS: CAVI level was 8.22 ± 0.18 m/s in diabetic CKD patients and significantly higher than in nondiabetic CKD (7.61 ± 0.18 m/s) and control (7.59 ± 0.17 m/s) patients. FGF-23 level was higher in the CKD groups than controls but not statistically significant. MCP-1 level was significantly higher in diabetic CKD patients. Klotho and sclerostin levels were significantly lower in diabetic CKD patients. In the whole cohort, CAVI showed positive correlations with age (r = 0.447, p < 0.0001), smoking (r = 0.331, p = 0.035), mean arterial blood pressure (MABP; r = 0.327, p < 0.0001), fasting blood glucose (r = 0.185, p = 0.033), and HbA1c (r = 0.258, p = 0.003). Stepwise regression analysis revealed that age (p = 0.0001, B = 0.461), MABP (p < 0.0001, B = 0.365), HbA1c (p = 0.003, B = 0.251), and MCP-1 (p = 0.013, B = 0.214) independently predicted CAVI levels. CONCLUSION: Our results indicate higher CAVI levels, therefore, resulting in increased arterial stiffness in the setting of diabetic CKD. Apart from age and MABP, deranged metabolic status, especially increased HbA1c and MCP-1 levels, is also independently associated with increasing CAVI levels in CKD patients. These results emphasize the importance of metabolic control in the development of arterial stiffness in CKD patients, which is an early predictor of developing cardiovascular complications.en_US
dc.language.isoenen_US
dc.relation.ispartofInternational urology and nephrologyen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.titleCardio-ankle vascular index is linked to deranged metabolic status, especially high HbA1c and monocyte-chemoattractant-1 protein, in predialysis chronic kidney disease.en_US
dc.typeArticleen_US
dc.identifier.volume52en_US
dc.identifier.issue1en_US
dc.identifier.startpage137-145
dc.identifier.startpageLID - 10.1007/s11255-019-02336-6 [doi]
dc.identifier.startpage137en_US
dc.identifier.endpage145en_US
dc.identifier.endpageLIDen_US
dc.authorid0000-0003-2251-0071-
dc.identifier.doi10.1007/s11255-019-02336-6-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.pmid31773386en_US
dc.identifier.scopus2-s2.0-85075569428en_US
dc.identifier.wosWOS:000512074300015en_US
dc.identifier.scopusqualityQ2-
dc.ownerPamukkale University-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeArticle-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
crisitem.author.dept14.02. Internal Medicine-
crisitem.author.dept14.02. Internal Medicine-
crisitem.author.dept14.02. Internal Medicine-
crisitem.author.dept14.03. Basic Medical Sciences-
crisitem.author.dept14.03. Basic Medical Sciences-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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