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Chronic kidney disease (CKD) patients are prone to a higher cardiovascular morbidity and mortality compared with the general population [1]. Consistent results from the basic and clinical research showed that cardiovascular susceptibility in CKD is due, partially at least, to a considerable acceleration of the vascular ageing processes in the context of chronic kidney disease-mineral bone disorder syndrome (CKD-MBD) [2]. This premature cardiovascular senescence is mainly characterized by altered endothelial reactivity, followed by pathologic calcification of cardiac valves and medial layer in the arteries [3]. The consequent increase of arterial stiffness worsens the cardiac afterload, contributing to the onset of left ventricular hypertrophy and to the progressive increase of pulse pressure (PP) leading to a significant reduction of diastolic tissue perfusion. The metabolic pathways linked to this premature ageing involve the dysregulation of several systems such as inflammation, oxydative stress, insulin resistance and mineral metabolism [3]. The alterations of calcium (Ca) and phosphate (P) homeostasis in renal patients, mainly driven by a derangement of Klotho/fibroblast growth factor 23 (FGF23)—parathormone (PTH)—vitamin D axis, are considered pivotal triggers and regulators of vascular ageing rather than mere biomarkers of CKD-MBD syndrome [3]. Thus, P overload and hyperparathyroidism are well known targets of medical treatments, such as P binders, vitamin D and calcimimetics, although with still limited evidence-based advantages in terms of survival in renal patients [3, 4]. The tough hedge that is still keeping nephrologists far from a conclusive and winning approach against vascular ageing is reasonably related to the still partial comprehension of the molecular pathways involved in a so complex, multifactorial and extreme process. New biomarkers and new actors are thus needed to orient the scientific knowledge towards further intervention strategies against CKD-MBD.