In addition to elevated blood pressure, there are several other postulated pathophysiological drivers of increased arterial stiffness in CKD such as activation of the renin-angiotensin-aldosterone system (RAAS), build-up of uraemic toxins, disordered bone and mineral metabolism (CKD-MBD), accumulation of advanced glycation end-products, chronic inflammation and oxidative stress which adversely affect endothelial function and calcific remodelling of the vessel wall [12, 129]. Here, REN is linked to chronic kidney disease.