Cardiovascular risk in children with chronic kidney disease (CKD) is many times higher compared to their healthy peers, and discovered in year 2000 fibroblast growth factor 23 (FGF23) may be one of the factors responsible. FGF23 together with its cofactor, α-Klotho protein, plays a pivotal role in calcium-phosphorus metabolism in patients with CKD by decreasing secretion of active metabolite of vitamin D and antagonizing phosphate resorption in renal tubules. Studies conducted in recent years revealed that FGF23 directly binds to its receptor on cardiomyocytes and promotes left ventricular hypertrophy. Clinical trials in children with CKD, similarly to adult studies, suggest a key role of this protein in development of calciumphosphorus disturbances. Single studies in small patient groups suggest also a significance of FGF23 in pathogenesis of cardiovascular alterations in this population. Further clinical trials investigating role of FGF23 in development of cardiovascular damage in larger groups of children are necessary, which may open new therapeutic options for these patients in future.
Keywords: cardiovascular risk; children; chronic kidney disease; fibroblast growth factor 23.
© 2016 MEDPRESS.