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End-stage kidney failure in hemodialysis patients is the pathological entity most associated with accelerated arterial aging. More recently, a link has been established between arterial stiffness and coagulation. The pathophysiology is characterized by early endothelial damage, a common feature of these two phenotypes. At a later stage of kidney disease, arterial stiffness develops, alongside atherothrombotic lesions. This results in a biological profile typical of a pro-thrombotic state. Anticoagulant therapy is not justified in primary prevention, due to the inherent hemorrhagic risk associated with kidney disease. For this reason, the thrombotic and hemorrhagic risk of kidney disease has not yet been translated into clear therapeutic recommendations for either arterial stiffness or coagulation. In this review, we will address the clinical and biological issues of such a mechanistic association.