22 research outputs found
FGF-23 associated with the progression of coronary artery calcification in hemodialysis patients
Serum uric acid is associated with high blood pressure in pediatric hemodialysis patients.
Malnutrition-inflammation-coronary calcification in pediatric patients receiving chronic hemodialysis
Elevated FGF 23 and phosphorus are associated with coronary calcification in hemodialysis patients
Fibroblast Growth Factor-23 Levels Are Associated with Vascular Calcifications in Peritoneal Dialysis Patients
Calcification of coronary arteries and abdominal aorta in relation to traditional and novel risk factors of atherosclerosis in hemodialysis patients
Fibroblast growth factor-23 and calcium phosphate product in young chronic kidney disease patients: a cross-sectional study
Deviations from the expected relationship between serum FGF23 and other markers in children with CKD: a cross-sectional study
Beyond mineral metabolism, is there an interplay between FGF23 and vitamin D in innate immunity?
Fibroblast growth factor 23 (FGF23) is an "endocrine" FGF acting in the kidney as a phosphaturic hormone and a suppressor of active vitamin D, through an inhibition of the 1α hydroxylase and a stimulation of the 24 hydroxylase. Beyond its well-known effects on the bone/kidney/parathyroid axis and its deregulation during chronic kidney disease (CKD), recent evidence has revealed its direct systemic effects on cardiovascular health. In the meantime, studies have highlighted the health implications for vitamin D inside and outside CKD that also extend beyond its classical actions on mineral homeostasis and bone metabolism: vitamin D has indeed been shown to exert pluripotent non-classical effects as a modulator of immune function in monocytes, mainly through the stimulation of the antimicrobial cathelicidin. The aim of this review is to provide new insights on the interplay between FGF23 and vitamin D in innate immunity in the context of CKD.</p
