Abstract
Cardiovascular diseases (CVD) are a hallmark in pediatric patients with chronic kidney disease (CKD) contributing to an enhanced risk of all-cause and CV morbidity and mortality in these patients. The bone-derived phosphaturic hormone fibroblast growth factor (FGF) 23 progressively rises with declining kidney function to maintain phosphate homeostasis, with up to 1,000-fold increase in patients with kidney failure requiring dialysis. FGF23 is associated with the development of left ventricular hypertrophy (LVH) and thereby accounts to be a CVD risk factor in CKD. Experimentally, FGF23 directly induces hypertrophic growth of cardiac myocytes in vitro and LVH in vivo. Further, clinical studies in adult CKD have observed cardiotoxicity associated with FGF23. Data regarding prevalence and determinants of FGF23 excess in children with CKD are limited. This review summarizes current data and discusses whether FGF23 may be a key driver of LVH in pediatric CKD.
Highlights
Chronic kidney disease (CKD) is a significant global health issue and defined as gradual loss of kidney function leading to irreversible kidney damage [1]
Increased level of circulating tumor necrosis factor-α (TNF-α) are observed in myocardial dysfunction and fibrosis and it is thought to be involved in the development of atherosclerosis by impairing endothelial function [39]
Numerous studies have observed a correlation of increased parathyroid hormone (PTH) levels and the progression of Left ventricular hypertrophy (LVH) in children with CKD stages 2–4 with PTH having a direct effect on cardiac myocytes [45, 46]
Summary
Chronic kidney disease (CKD) is a significant global health issue and defined as gradual loss of kidney function leading to irreversible kidney damage [1]. CKD patients present a high risk for cardiovascular events. Fifty percent which remain the predominant cause of patients with CKD stage 4 and 5 develop cardiovascular diseases (CVD), which cause of death with 40% mortality rate [2]. Left ventricular hypertrophy (LVH), cardiac fibrosis and vascular diseases remain the most common cardiac abnormalities in CRS 4, with 90% of adult patients with kidney failure developing LVH [5, 6]. Childhood CKD is associated with amplified cardiovascular (CV) morbidity and mortality both during childhood with progressive worsening in those with childhood-onset CKD become young adults [7,8,9]. As LVH and its progression are associated with adverse CV outcomes in patients with CKD [15], it remains important to understand additional risk factors. The present narrative review focusses on FGF23, a bone-derived phosphaturic hormone regulating renal phosphate homeostasis, in the development of LVH in pediatric CKD and summarizes recent clinical literature in this field
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