Abstract
In patients with chronic kidney disease（CKD）, particularly those on hemodialysis, the cardiovascular mortality rate is extremely high. Polyvascular diseases develop at an early stage of CKD. The pathophysiology includes insulin resistance and/or imbalance between nitric oxide（NO）and endothelin bioavailability, as well as oxidative stress. Pathophysiologies, such as hemorheological disarrangement, may be overlooked because of hyperfibrinogenemia and the higher rate of production of monocyte-platelet complexes in circulation, which plays an important role in atherosclerosis. Regarding clinical findings, most nephrologists understand the importance of coronary artery disease, but few are aware of the deleterious influence of peripheral arterial disease（PAD）on prognosis for CKD patients, which is known to be an independent risk factor for PAD. An understanding of the pathophysiology behind vascular calcification and strategic treatment are critical to achieve a favorable outcome for CKD patients. In this regard, FGF-23 and associated factors together with Klotho molecules play an important role. In this article, we review cardiovascular diseases in CKD patients with an emphasis on the clinical aspects of polyvascular disease. Finally, we will address how to detect microcirculatory impairment and eradicate vascular calcification as early as possible prior to renal replacement therapy. The FGF-23-Klotho gene axis, and vitamin D and phosphate control should be carefully investigated.
