Fibroblast growth factor 23 is not associated with and does not induce arterial calcification.
Date
2013-06
Journal Title
Journal ISSN
Volume Title
Repository Usage Stats
views
downloads
Citation Stats
Abstract
Elevated fibroblast growth factor 23 (FGF23) is associated with cardiovascular disease in patients with chronic kidney disease. As a potential mediating mechanism, FGF23 induces left ventricular hypertrophy; however, its role in arterial calcification is less clear. In order to study this, we quantified coronary artery and thoracic aorta calcium by computed tomography in 1501 patients from the Chronic Renal Insufficiency Cohort (CRIC) study within a median of 376 days (interquartile range 331-420 days) of baseline. Baseline plasma FGF23 was not associated with the prevalence or severity of coronary artery calcium after multivariable adjustment. In contrast, higher serum phosphate levels were associated with prevalence and severity of coronary artery calcium, even after adjustment for FGF23. Neither FGF23 nor serum phosphate were consistently associated with thoracic aorta calcium. We could not detect mRNA expression of FGF23 or its coreceptor, klotho, in human or mouse vascular smooth muscle cells, or normal or calcified mouse aorta. Whereas elevated phosphate concentrations induced calcification in vitro, FGF23 had no effect on phosphate uptake or phosphate-induced calcification regardless of phosphate concentration or even in the presence of soluble klotho. Thus, in contrast to serum phosphate, FGF23 is not associated with arterial calcification and does not promote calcification experimentally. Hence, phosphate and FGF23 promote cardiovascular disease through distinct mechanisms.
Type
Department
Description
Provenance
Subjects
Citation
Permalink
Published Version (Please cite this version)
Publication Info
Scialla, Julia J, Wei Ling Lau, Muredach P Reilly, Tamara Isakova, Hsueh-Ying Yang, Matthew H Crouthamel, Nicholas W Chavkin, Mahboob Rahman, et al. (2013). Fibroblast growth factor 23 is not associated with and does not induce arterial calcification. Kidney international, 83(6). pp. 1159–1168. 10.1038/ki.2013.3 Retrieved from https://hdl.handle.net/10161/18486.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
Collections
Scholars@Duke
Julia Jarrard Scialla
Dr. Scialla is an Associate Professor of Medicine in Nephrology at Duke University and a faculty member at the Duke Clinical Research Institute. Dr. Scialla trained in Internal Medicine, Nephrology, and Clinical Epidemiology at the Johns Hopkins University School of Medicine and the Johns Hopkins Bloomberg School of Public Health. Her research focuses on chronic kidney disease (CKD) epidemiology and prevention, with an emphasis on the role of metabolic complications and nutrition. Current studies are focused on treatment and prevention of abnormal phosphate homeostasis, acid-base physiology, diabetic and other forms of kidney disease, and outcomes in end-stage kidney disease.
Dr. Scialla’s work engages a number of study designs including prospective cohort studies, observational comparative effectiveness studies, and patient-oriented physiologic studies. She has worked closely with multiple chronic disease cohorts including the Chronic Renal Insufficiency Cohort (CRIC) Study, the African American Study of Kidney Disease and Hypertension (AASK), the Jackson Heart Study (JHS), and secondary analyses in clinical trials. Studies in electronic health records (EHR) and registries have engaged dialysis EHR data, the United States Renal Data System, and public registries, such as the National Health and Nutrition Examination Survey. Physiologic studies include the Acid Base Complication in CKD Study, secondary analyses in the DASH Mechanism Study, and the newly launched MURDOCK Kidney Health Study.
Myles Selig Wolf
The focus of my research is disordered mineral metabolism across the spectrum of chronic kidney disease, including dialysis, kidney transplantation and earlier stages.
My research has been published in leading general medicine and subspecialty journals, including the New England Journal of Medicine, JAMA, the Journal of Clinical Investigation, Circulation, Cell Metabolism, Journal of the American Society of Nephrology, and Kidney International, among others.
My primary contributions have been in the area of hormonal regulation of phosphate homeostasis. I have helped to characterize the physiological role of fibroblast growth factor 23 in health and in chronic kidney disease, and the impact of elevated fibroblast growth factor 23 levels on adverse clinical outcomes in patients with kidney disease.
Unless otherwise indicated, scholarly articles published by Duke faculty members are made available here with a CC-BY-NC (Creative Commons Attribution Non-Commercial) license, as enabled by the Duke Open Access Policy. If you wish to use the materials in ways not already permitted under CC-BY-NC, please consult the copyright owner. Other materials are made available here through the author’s grant of a non-exclusive license to make their work openly accessible.