The pathophysiology of atherosclerosis in patients with CKD arises not from a single factor but from multiple factors, and it is thought that both risk factors that induce CKD such as diabetes or hypertension and mechanisms that are further exacerbated in CKD, such as chronic inflammation derived from activation of the PlGF/Flt-1 pathway, vascular endothelial damage due to the renin-angiotensin system, or sympathetic nerve stimulation and the dysregulation of calcium and phosphorus, are involved20,21. This evidence concerns the gene PGF and hypertensive disorder.