Growth differentiation factor-15 and fibroblast growth factor-23 are associated with mortality in type 2 diabetes – An observational follow-up study

Two biomarkers, growth differentiation factor 15 (GDF-15) and fibroblast growth factor 23 (FGF-23)), reflecting different aspects of renal pathophysiology, were evaluated as determinants of decline in estimated glomerular filtration rate (eGFR), incident cardiovascular disease (CVD) and all-cause mo...

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Veröffentlicht in:	PloS one Jg. 13; H. 4; S. e0196634
Hauptverfasser:	Frimodt-Møller, Marie, von Scholten, Bernt Johan, Reinhard, Henrik, Jacobsen, Peter Karl, Hansen, Tine Willum, Persson, Frederik Ivar, Parving, Hans-Henrik, Rossing, Peter
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 26.04.2018 Public Library of Science (PLoS)
Schlagworte:	Aged Albuminuria - complications Albuminuria - diagnosis Analysis Biology and Life Sciences Biomarkers Cardiovascular diseases Cardiovascular Diseases - diagnosis Cardiovascular Diseases - epidemiology Cardiovascular Diseases - etiology Cause of Death Coronary artery disease Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - mortality Diabetes Mellitus, Type 2 - pathology Differentiation Epidermal growth factor receptors Female Fibroblast growth factor 23 Fibroblast growth factors Fibroblast Growth Factors - blood Follow-Up Studies Glomerular Filtration Rate Growth Differentiation Factor 15 - blood Heart diseases Humans Incidence Kaplan-Meier Estimate Kidneys Male Mathematical models Medicine and Health Sciences Middle Aged Mortality Patients Proportional Hazards Models Renal function Renal Insufficiency, Chronic - diagnosis Renal Insufficiency, Chronic - etiology Risk analysis Risk Factors Type 2 diabetes Denmark United States > US
ISSN:	1932-6203, 1932-6203
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Zusammenfassung:	Two biomarkers, growth differentiation factor 15 (GDF-15) and fibroblast growth factor 23 (FGF-23)), reflecting different aspects of renal pathophysiology, were evaluated as determinants of decline in estimated glomerular filtration rate (eGFR), incident cardiovascular disease (CVD) and all-cause mortality in patients with type 2 diabetes (T2D) and microalbuminuria, but without clinical cardiac disease. Prospective study including 200 T2D patients. The predefined endpoint of chronic kidney disease (CKD) progression: A decline in eGFR of >30% at any time point during follow-up. Hazard ratios (HR) are provided per 1 SD increment of log2-transformed values. Mean (± SD) age was 59 ± 9 years, eGFR 91.1 ± 18.3 ml/min/1.73m2 and median (IQR) UAER 103 (39-230) mg/24-h. During a median 6.1 years follow-up, 40 incident CVD events, 26 deaths and 42 patients reached the CKD endpoint after median 4.9 years. Higher GDF-15 was a determinant of decline in eGFR >30% and all-cause mortality in adjusted models (HR 1.7 (1.1-2.5); p = 0.018 and HR 1.9 (1.2-2.9); p = 0.003, respectively). Adding GDF-15 to traditional risk factors improved risk prediction of decline in renal function (relative integrated discrimination improvement (rIDI) = 30%; p = 0.037). Higher FGF-23 was associated with all-cause mortality in adjusted models (HR 1.6 (1.1-2.2); p = 0.011) with a rIDI of 30% (p = 0.024). In patients with T2D and microalbuminuria, higher GDF-15 and FGF-23 were independently associated with all-cause mortality and higher GDF-15 improved risk prediction of decline in kidney function and higher FGF-23 of all-cause mortality, beyond traditional risk factors, but not independently of GDF-15.
Bibliographie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 Competing Interests: FP reports having received research grants from AstraZeneca and Novartis and lecture fees from Novartis, Eli Lilly, MSD, AstraZeneca, Sanofi and Boehringer Ingelheim and having served as a consultant for Astra Zeneca, Bayer, Amgen, Novo Nordisk and MSD. PR received lecture fees from Bayer and Boehringer Ingelheim, and research grants from Novartis, Astra Zeneca, Novo Nordisk and has served as a consultant for Bayer, Astra Zeneca, Boehringer Ingelheim, AbbVie, Novo Nordisk (all honoraria to his institution) and reports having equity interest in Novo Nordisk. This does not alter our adherence to PLOS ONE policies on sharing data and materials. The results presented in this paper have not been published previously in whole or part, except in abstract format.
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0196634