Cardiovascular events in chronic kidney disease (CKD)—an importance of vascular calcification and microcirculatory impairment

In patients with chronic kidney disease (CKD), particularly in patients with hemodialysis, cardiovascular mortality rate is extremely high. Polyvascular diseases develop at an early stage of CKD. Pathophysiology includes insulin resistance and/or imbalance between nitric oxide (NO) and endothelin bioavailability as well as oxidative stress. Overlooked pathophysiology may be hemorheological disarrangement because of hyperfibrinogenemia, and higher rate of production for monocyte-platelet complexes in circulation, which plays an important role for atherosclerosis. In terms of clinical findings, most of nephrologists have already known about the importance of coronary artery disease, while few of nephrologists are aware of devastating influence of peripheral arterial disease (PAD) on prognosis for the patients with CKD which is known to be one of the independent risk factors for PAD. The understanding in pathophysiology of vascular calcification and strategic treatment is a critical issue to achieve favorable outcome for the patients with CKD. In this regard, FGF-23 and associated factors together with Klotho molecules play an important role.