Shilpa Sharma1, Ronit Katz2, Ruth F Dubin3, David A Drew4, Orlando M Gutierrez5, Michael G Shlipak3, Mark J Sarnak4, Joachim H Ix6. 1. Division of Nephrology, David Geffen School of Medicine at UCLA and VA Greater Los Angeles Healthcare System, Los Angeles, California, USA. 2. Department of Obstetrics and Gynecology, University of Washington, Seattle, Washington, USA. 3. Kidney Health Research Collaborative, University of California San Francisco, San Francisco, California, USA. 4. Division of Nephrology, Department of Medicine, Tufts Medical Center, Boston, Massachusetts, USA. 5. Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA. 6. Division of Nephrology-Hypertension, University of California San Diego and Veteran Affairs San Diego Healthcare System, San Diego, California, USA.
Abstract
OBJECTIVES: Fibroblast growth factor (FGF)-23 is a key regulator of mineral metabolism and has been linked with left ventricular hypertrophy in animal models. Most existing epidemiologic studies evaluated a C-terminal FGF23 assay which measures both the intact (active) hormone and inactive fragments. The relationship of intact FGF23 with cause-specific mortality is unknown. DESIGN: Prospective analyses of data from Health, Aging, & Body Composition (HABC) study. SETTING: Community-living adults aged 70 to 79 years with longitudinal follow up.
OBJECTIVES: Fibroblast growth factor (FGF)-23 is a key regulator of mineral metabolism and has been linked with left ventricular hypertrophy in animal models. Most existing epidemiologic studies evaluated a C-terminal FGF23 assay which measures both the intact (active) hormone and inactive fragments. The relationship of intact FGF23 with cause-specific mortality is unknown. DESIGN: Prospective analyses of data from Health, Aging, & Body Composition (HABC) study. SETTING: Community-living adults aged 70 to 79 years with longitudinal follow up.
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