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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.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentBiyoistatistik Ana Bilim Dalı
dc.contributor.departmentKardiyoloji Ana Bilim Dalı
dc.contributor.departmentİç Hastalıkları Ana Bilim Dalı
dc.contributor.departmentBiyokimya Ana Bilim Dalı
dc.contributor.departmentNefroloji Ana Bilim Dalı
dc.contributor.orcid0000-0003-2589-8585
dc.contributor.orcid0000-0002-0710-0923
dc.contributor.orcid0000-0001-8404-8252
dc.contributor.orcid0000-0003-2467-9356
dc.contributor.researcheridHLG-6346-2023
dc.contributor.researcheridI-7575-2015
dc.contributor.researcheridAAH-5054-2021
dc.contributor.researcheridAAH-4002-2021
dc.contributor.researcheridABE-4424-2022
dc.contributor.researcheridAAW-9185-2020
dc.contributor.researcheridA-7063-2018
dc.contributor.scopusid23988796000
dc.contributor.scopusid35612977100
dc.contributor.scopusid55858507600
dc.contributor.scopusid55371331300
dc.contributor.scopusid57197017096
dc.contributor.scopusid56399188100
dc.contributor.scopusid55134803100
dc.contributor.scopusid15832295800
dc.contributor.scopusid57204660708
dc.contributor.scopusid6602684544
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.
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.endpage449
dc.identifier.issn1735-8582
dc.identifier.issue6
dc.identifier.pubmed25362218
dc.identifier.scopus2-s2.0-84908363960
dc.identifier.startpage443
dc.identifier.urihttps://hdl.handle.net/11452/39873
dc.identifier.volume8
dc.identifier.wos000345554400003
dc.indexed.wosSCIE
dc.language.isoen
dc.publisherIranian Soc Nephrolgy
dc.relation.collaborationSanayi
dc.relation.journalIranian Journal of Kidney Diseases
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectArterial stiffness
dc.subjectFibroblast growth factor 23
dc.subjectAutosomal dominant polycystic kidney disease
dc.subjectStage renal-disease
dc.subjectEndothelial dysfunction
dc.subjectHeart
dc.subjectNormotensive patients
dc.subjectUrology & nephrology
dc.subjectMortality
dc.subjectResistance
dc.subjectKlotho
dc.subjectMouse
dc.subjectInflammation
dc.subject.emtreeAdult
dc.subject.emtreeArterial stiffness
dc.subject.emtreeArtery disease
dc.subject.emtreeArticle
dc.subject.emtreeAutosomal dominant disorder
dc.subject.emtreeBlood pressure
dc.subject.emtreeBlood vessel compliance
dc.subject.emtreeBody mass
dc.subject.emtreeCardiovascular parameters
dc.subject.emtreeCardiovascular risk
dc.subject.emtreeChronic kidney disease
dc.subject.emtreeControlled study
dc.subject.emtreeCoronary artery disease
dc.subject.emtreeFemale
dc.subject.emtreeGlomerulus filtration rate
dc.subject.emtreeHuman
dc.subject.emtreeHypertension
dc.subject.emtreeKidney polycystic disease
dc.subject.emtreeLarge arterial elasticity index
dc.subject.emtreeMajor clinical study
dc.subject.emtreeMale
dc.subject.emtreePhosphaturia
dc.subject.emtreePulse wave
dc.subject.emtreeSmall arterial elasticity index
dc.subject.emtreeUrea blood level
dc.subject.emtreeArtery
dc.subject.emtreeBlood
dc.subject.emtreeCompliance (physical)
dc.subject.emtreeElasticity
dc.subject.emtreeKidney polycystic disease
dc.subject.emtreePathophysiology
dc.subject.emtreePhysiology
dc.subject.emtreeRegression analysis
dc.subject.emtree25 hydroxyvitamin d
dc.subject.emtreeCalcium
dc.subject.emtreeCholesterol
dc.subject.emtreeCreatinine
dc.subject.emtreeFibroblast growth factor 23
dc.subject.emtreeGlucose
dc.subject.emtreeHigh density lipoprotein cholesterol
dc.subject.emtreeKlotho protein
dc.subject.emtreeLow density lipoprotein cholesterol
dc.subject.emtreePhosphate
dc.subject.emtreeTriacylglycerol
dc.subject.emtreeUric acid
dc.subject.emtreeFibroblast growth factor
dc.subject.emtreeFibroblast growth factor 23
dc.subject.meshAdult
dc.subject.meshArteries
dc.subject.meshCompliance
dc.subject.meshElasticity
dc.subject.meshFemale
dc.subject.meshFibroblast growth factors
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshPolycystic kidney, autosomal dominant
dc.subject.meshPulse wave analysis
dc.subject.meshRegression analysis
dc.subject.wosUrology & nephrology
dc.titleArterial dysfunction in early autosomal dominant polycystic kidney disease independent of fibroblast growth factor 23
dc.typeArticle
dc.wos.quartileQ4 (Urology & Nephrology)
dspace.entity.typePublication
local.contributor.departmentTıp Fakültesi/Nefroloji Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/Biyokimya Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/İç Hastalıkları Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/Kardiyoloji Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/Biyoistatistik Ana Bilim Dalı
local.indexed.atWOS
local.indexed.atScopus
local.indexed.atPubMed

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