Vascular calcification (VC) represents one of the major complications of chronic kidney disease (CKD) and is characterised by an active, tightly regulated process of hydroxyapatite crystal deposition within the arterial wall and cardiac valves. In advanced CKD, VC plays a central role in promoting arterial stiffness, left ventricular overload, and the high cardiovascular mortality typical of this population. The distinction between intimal and medial forms, as well as between vascular and valvular calcification, holds key diagnostic and therapeutic implications. VC occurs within the broader framework of CKD–mineral and bone disorder (CKD–MBD), in which disturbances of mineral metabolism, chronic inflammation, and osteogenic trans-differentiation of vascular cells act synergistically. Current therapeutic strategies aim to restore the balance between promoters and inhibitors of mineralisation by targeting mineral metabolism, oxidative stress, and cellular and molecular pathways. Future perspectives include integrated and personalised approaches, together with novel agents designed to modulate crystal formation and reactivate physiological inhibitors, thereby enhancing vascular resilience in CKD.