Arterial dysfunction in early autosomal dominant polycystic kidney disease independent of fibroblast growth factor 23

dc.contributor.authorYıldız, Abdülmecit
dc.contributor.authorKaraaǧaç, Kemal
dc.contributor.authorDoğan, İbrahim
dc.contributor.buuauthorGül, Bülent Cuma
dc.contributor.buuauthorErsoy, Alparslan
dc.contributor.buuauthorAsiltaş, Burak
dc.contributor.buuauthorErmurat, Selime
dc.contributor.buuauthorDoğan, Selda
dc.contributor.buuauthorOruç, Ayşegül
dc.contributor.buuauthorSağ, Saim
dc.contributor.buuauthorOcakoĝlu, Gökhan
dc.contributor.buuauthorAktaş, Nimet
dc.contributor.buuauthorGüllülü, Sümeyye
dc.contributor.buuauthorGüllülü, Mustafa
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Nefroloji Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/İç Hastalıkları Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Kardiyoloji Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Biyoistatistik Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0003-2589-8585tr_TR
dc.contributor.orcid0000-0002-0710-0923tr_TR
dc.contributor.orcid0000-0001-8404-8252tr_TR
dc.contributor.orcid0000-0003-2467-9356tr_TR
dc.contributor.researcheridHLG-6346-2023tr_TR
dc.contributor.researcheridI-7575-2015tr_TR
dc.contributor.researcheridAAH-5054-2021tr_TR
dc.contributor.researcheridAAH-4002-2021tr_TR
dc.contributor.researcheridABE-4424-2022tr_TR
dc.contributor.researcheridAAW-9185-2020tr_TR
dc.contributor.researcheridA-7063-2018tr_TR
dc.contributor.scopusid23988796000tr_TR
dc.contributor.scopusid35612977100tr_TR
dc.contributor.scopusid55858507600tr_TR
dc.contributor.scopusid55371331300tr_TR
dc.contributor.scopusid57197017096tr_TR
dc.contributor.scopusid56399188100tr_TR
dc.contributor.scopusid55134803100tr_TR
dc.contributor.scopusid15832295800tr_TR
dc.contributor.scopusid57204660708tr_TR
dc.contributor.scopusid6602684544tr_TR
dc.date.accessioned2024-02-20T12:49:49Z
dc.date.available2024-02-20T12:49:49Z
dc.date.issued2014-11
dc.description.abstractIntroduction. Recent studies report reduced vascular compliance and elevated levels of fibroblast growth factor 23 (FGF23) in patients with autosomal dominant polycystic kidney disease (ADPKD) and preserved kidney function. In the present study, we investigated the relationship between vascular compliance and FGF23 in patients in early phases of ADPKD. Materials and Methods. We studied 54 ADPKD patients with preserved kidney function and 24 healthy individuals. All participants underwent noninvasive pulse wave analysis in order to determine large arterial elasticity index (LAEI) and small arterial elasticity index (SAEI) using a modified Windkessel model. Levels of FGF23 in addition to several cardiovascular risk factors were evaluated. Linear regression analyses were performed to determine independent correlates of LAEI, SAEI, and FGF23. Results. In the ADPKD group, 33 patients were hypertensive and the remaining patients were normotensive. Serum FGF23 levels of both ADPKD groups were significantly higher than that in the controls. Both hypertensive and normotensive ADPKD patients had lower LAEI and SAEI levels compared to the controls. There was no significant correlation between vascular compliance parameters and FGF23 levels. Having ADPKD was independently associated with increased FGF23 levels and decreased SAEI. Conclusions. Fibroblast growth factor 23 was found substantially elevated and arterial compliance was found significantly decreased in early ADPKD patients regardless of hypertension. However, there was no significant correlation between FGF23 levels and arterial function parameters. Additional studies are required to determine possible mechanisms of these disturbances and cardiovascular effects of FGF23 in ADPKD patients.en_US
dc.identifier.citationYıldız, A.. vd. (2014). "Arterial dysfunction in early autosomal dominant polycystic kidney disease independent of fibroblast growth factor 23". Iranian Journal of Kidney Diseases, 8(6), 443-449.
dc.identifier.eissn1735-8604
dc.identifier.endpage449tr_TR
dc.identifier.issn1735-8582
dc.identifier.issue6tr_TR
dc.identifier.pubmed25362218tr_TR
dc.identifier.scopus2-s2.0-84908363960tr_TR
dc.identifier.startpage443tr_TR
dc.identifier.urihttps://hdl.handle.net/11452/39873en_US
dc.identifier.volume8tr_TR
dc.identifier.wos000345554400003tr_TR
dc.indexed.wosSCIEen_US
dc.language.isoenen_US
dc.publisherIranian Soc Nephrolgyen_US
dc.relation.collaborationSanayitr_TR
dc.relation.journalIranian Journal of Kidney Diseasesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectArterial stiffnessen_US
dc.subjectFibroblast growth factor 23en_US
dc.subjectAutosomal dominant polycystic kidney diseaseen_US
dc.subjectStage renal-diseaseen_US
dc.subjectEndothelial dysfunctionen_US
dc.subjectHearten_US
dc.subjectNormotensive patientsen_US
dc.subjectUrology & nephrologyen_US
dc.subjectMortalityen_US
dc.subjectResistanceen_US
dc.subjectKlothoen_US
dc.subjectMouseen_US
dc.subjectInflammationen_US
dc.subject.emtreeAdulten_US
dc.subject.emtreeArterial stiffnessen_US
dc.subject.emtreeArtery diseaseen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeAutosomal dominant disorderen_US
dc.subject.emtreeBlood pressureen_US
dc.subject.emtreeBlood vessel complianceen_US
dc.subject.emtreeBody massen_US
dc.subject.emtreeCardiovascular parametersen_US
dc.subject.emtreeCardiovascular risken_US
dc.subject.emtreeChronic kidney diseaseen_US
dc.subject.emtreeControlled studyen_US
dc.subject.emtreeCoronary artery diseaseen_US
dc.subject.emtreeFemaleen_US
dc.subject.emtreeGlomerulus filtration rateen_US
dc.subject.emtreeHumanen_US
dc.subject.emtreeHypertensionen_US
dc.subject.emtreeKidney polycystic diseaseen_US
dc.subject.emtreeLarge arterial elasticity indexen_US
dc.subject.emtreeMajor clinical studyen_US
dc.subject.emtreeMaleen_US
dc.subject.emtreePhosphaturiaen_US
dc.subject.emtreePulse waveen_US
dc.subject.emtreeSmall arterial elasticity indexen_US
dc.subject.emtreeUrea blood levelen_US
dc.subject.emtreeArteryen_US
dc.subject.emtreeBlooden_US
dc.subject.emtreeCompliance (physical)en_US
dc.subject.emtreeElasticityen_US
dc.subject.emtreeKidney polycystic diseaseen_US
dc.subject.emtreePathophysiologyen_US
dc.subject.emtreePhysiologyen_US
dc.subject.emtreeRegression analysisen_US
dc.subject.emtree25 hydroxyvitamin den_US
dc.subject.emtreeCalciumen_US
dc.subject.emtreeCholesterolen_US
dc.subject.emtreeCreatinineen_US
dc.subject.emtreeFibroblast growth factor 23en_US
dc.subject.emtreeGlucoseen_US
dc.subject.emtreeHigh density lipoprotein cholesterolen_US
dc.subject.emtreeKlotho proteinen_US
dc.subject.emtreeLow density lipoprotein cholesterolen_US
dc.subject.emtreePhosphateen_US
dc.subject.emtreeTriacylglycerolen_US
dc.subject.emtreeUric aciden_US
dc.subject.emtreeFibroblast growth factoren_US
dc.subject.emtreeFibroblast growth factor 23en_US
dc.subject.meshAdulten_US
dc.subject.meshArteriesen_US
dc.subject.meshComplianceen_US
dc.subject.meshElasticityen_US
dc.subject.meshFemaleen_US
dc.subject.meshFibroblast growth factorsen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPolycystic kidney, autosomal dominanten_US
dc.subject.meshPulse wave analysisen_US
dc.subject.meshRegression analysisen_US
dc.subject.wosUrology & nephrologyen_US
dc.titleArterial dysfunction in early autosomal dominant polycystic kidney disease independent of fibroblast growth factor 23en_US
dc.typeArticleen_US
dc.wos.quartileQ4 (Urology & Nephrology)en_US

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