Fibroblast growth factor 23 and cardiovascular disease in patients with chronic kidney disease

Abstract

Abstract Chronic kidney disease (CKD) has been known to be associated with an increased risk of cardiovascular (CV) mortality and morbidity in Japan. Although traditional risk factors contribute to the development of CV disease in CKD patients, they cannot fully explain the unacceptably high incidence of CV mortality. Recently, non-traditional risk factors, including abnormal mineral metabolism, have been suggested to be involved in the increased risk of CV events. The medical treatment of CKD-mineral bone disorders (CKD-MBD) has been associated with encouraging, but inconsistent, improvement in CV disease complications and patient survival. A better understanding of the biomarkers and mechanisms involved in left ventricular hypertrophy (LVH) and vascular calcification might improve the diagnosis and treatment of the CV disease secondary to CKD-MBD, thus improving patient survival. Recent insights into fibroblast growth factor 23 (FGF23) and its co-receptor, Klotho, have led to marked advancements in the interpretation of data about CKD-MBD and CV damage