Fibroblast growth factor FGF is a phosphaturic hormone that increases in early chronic kidney disease CKD before abnormalities in serum calcium, phosphate, or parathyroid hormone PTH become apparent [1, 2]. FGF is thought to be produced by altered osteocyte function in early CKD [3] and is elevated in patients with end-stage kidney disease. FGF has been linked with mortality, vascular calcification, markers of bone turnover, and left ventricular hypertrophy [4].
Cardiovascular disease is a major cause of morbidity and mortality in adult patients with end-stage renal disease receiving maintenance dialysis [5]. Cardiovascular mortality is also a significant issue in children and young adults with kidney disease, largely due to vascular calcifications in the media of vessels [6, 7].
As higher phosphate levels are associated with vascular calcifications, several studies have examined the role of serum FGF levels in phosphate metabolism and vascular calcifications.
However, there is no clear link between FGF levels and vascular calcifications. One study suggests that FGF concentrations in blood are not associated with aortic calcifications [9]. Other studies, however, have clearly linked vascular calcifications with FGF levels as an independent risk factor, even across all CKD stages [10]. In fact, children and young adult patients with calcifications on dialysis have higher serum phosphorus concentrations and a higher calcium-phosphorus ion product in serum [11].
Desjardins et al. FGF has also been associated with endothelial dysfunction [12, 13]. In addition to increased FGF production by osteocytes [3], FGF concentrations may also rise because of accumulation in the serum secondary to decreased glomerular filtration. FGF is a small molecular weight molecule, similar to that of Cystatin C CysC , which also accumulates in serum in patients with decreased renal clearance [14].
