Purpose of review
Cardiovascular disease is the leading cause of death in children and young adults with end-stage renal disease (ESRD). As adults, children with advanced chronic kidney disease (CKD) have extremely high prevalence of traditional and uremia-related cardiovascular risk factors. Coronary artery calcification is one of the earliest cardiovascular markers detected in children with ESRD. The purpose of this review is to examine the new developments in pathogenesis of coronary artery calcification and to describe recently published studies on this topic in children with CKD.
There is growing evidence that fibroblast growth factor 23 (FGF23) and Klotho factor play a key role in the development of coronary artery calcification in ESRD. Recent studies have shown that induction of vascular calcification begins in early normophosphatemic CKD by the reduction of vascular Klotho and increased FGF23 secretion. Pediatric studies confirmed the presence of abnormal FGF23 and Klotho metabolism and the association of increased circulating FGF23 with coronary artery calcification in children with CKD.
New developments in our understanding of the mechanisms of vascular calcification in patients with early CKD require further investigation of whether control of FGF23/Klotho metabolism will prevent or delay the development of coronary artery calcification and other cardiovascular outcomes.