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Titel: Strength of Fibroblast Growth Factor 23 as a Cardiovascular Risk Predictor in Chronic Kidney Disease Weaken by ProBNP Adjustment
VerfasserIn: Emrich, Insa E.
Brandenburg, Vincent
Sellier, Alexander B
Schauerte, Johanna
Wiedenroth, Johanna
Untersteller, Kathrin
Lennartz, Claudia S
Seiler-Mussler, Sarah
Wagenpfeil, Stefan
Fliser, Danilo
Heine, Gunnar H
Sprache: Englisch
Titel: American Journal of Nephrology.
Bandnummer: 49
Heft: 3
Seiten: 203–211
Verlag/Plattform: Karger
Erscheinungsjahr: 2019
Freie Schlagwörter: C-terminal fibroblast growth factor 23
Intact fibroblast growth factor 23
Iron deficiency
Heart failure
Cardiovascular events
DDC-Sachgruppe: 610 Medizin, Gesundheit
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: Background: Various epidemiological studies linked high fibroblast growth factor 23 (FGF23) levels with cardiovascular events in chronic kidney disease (CKD). It remains enigmatic whether high FGF23 exerts adverse cardiovascular effects, or whether it reflects detrimental effects of residual confounders. Earlier studies adjusted for CKD-mineral bone disease (CKD-MBD) regulators of FGF23 rather than for recently discovered non-CKD-MBD regulators, among which iron deficiency and heart failure are of particular importance. Moreover, they used c-terminal FGF23 (cFGF23) assays rather than more specific intact FGF23 (iFGF23) assays. Methods: The CARE FOR HOMe study analyzed plasma ferritin, iFGF23, cFGF23 and N-terminal proBNP (NT-proBNP) along with conventional risk factors, among 575 CKD G2-G4 patients to determine the interaction between FGF23, its non-CKD-MBD regulators, and incident cardiovascular events in CKD patients. The participants were followed up for 5.1 ± 2.1 years for the occurrence of atherosclerotic events and hospitalization for acute decompensated heart failure. Results: cFGF23 correlated strongly with high iFGF23 (r = 0.607), fairly with high NT-proBNP (r = 0.453) and weakly with low ferritin (r = –0.207); correlation coefficients of iFGF23 with NT-proBNP and ferritin were numerically lower. In Kaplan-Meier analyses, both endpoints were predicted by cFGF23 and iFGF23. In Cox regression models, cFGF23 remained an outcome predictor after adjustment for conventional risk factors and ferritin. This prediction was largely eliminated when further adjusting for NT-proBNP. iFGF23 was less consistently associated with adverse outcome in partly adjusted models, and failed to predict outcome in fully adjusted models. Conclusion: In summary, iron deficiency and heart failure affect plasma FGF23. As adjustment for NT-proBNP virtually eliminates the association between plasma FGF23 and predefined outcome, we speculate that high FGF23, rather than exerting detrimental cardiovascular effects, mirrors prevalent heart disease.
DOI der Erstveröffentlichung: 10.1159/000497125
URL der Erstveröffentlichung: https://karger.com/ajn/article/49/3/203/41592/Strength-of-Fibroblast-Growth-Factor-23-as-a
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-404640
hdl:20.500.11880/36376
http://dx.doi.org/10.22028/D291-40464
ISSN: 0250-8095
1421-9670
Datum des Eintrags: 4-Sep-2023
Fakultät: M - Medizinische Fakultät
Fachrichtung: M - Medizinische Biometrie, Epidemiologie und medizinische Informatik
M - Innere Medizin
Professur: M - Prof. Dr. Stefan Wagenpfeil
M - Prof. Dr. Michael Böhm
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes

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