Fujii Hideki, Joki Nobuhiko
Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Kobe, Japan.
Division of Nephrology, Toho University Ohashi Medical Center, 2-17-6 Ohashi, Meguro-Ku, Tokyo, 153-8515, Japan.
Clin Exp Nephrol. 2017 Mar;21(Suppl 1):53-63. doi: 10.1007/s10157-016-1363-8. Epub 2017 Jan 6.
The mineral bone disorder of CKD, called Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), has a major role in the etiology and progression of cardiovascular disease in CKD patients. Since the main emphasis in CKD-MBD is on three categories (bone abnormalities, laboratory abnormalities, and vascular calcifications), we have routinely accepted ectopic cardiovascular calcifications as a central risk factor in the pathophysiology of CKD-MBD for cardiac events. However, recent compelling evidence suggests that some CKD-MBD-specific factors other than vascular calcification might contribute to the onset of cardiovascular disease. Most notable is fibroblast growth factor-23 (FGF23), which is thought to be independently associated with cardiac remodeling. Slow progression of cardiac disorders, such as vascular calcification and cardiac remodeling, characterizes cardiac disease due to CKD-MBD. In contrast, fatal arrhythmia may be induced when QT prolongation occurs with CKD-MBD treatment, such as with lower Ca dialysate or the use of calcimimetics. Sudden onset of fatal cardiac events, such as heart failure and sudden cardiac death, due to fatal arrhythmia would be another distinctive phenomenon of CKD-MBD. This may be defined as CKD-MBD-specific cardiac complex syndrome.
慢性肾脏病的矿物质骨代谢紊乱,称为慢性肾脏病-矿物质和骨代谢紊乱(CKD-MBD),在慢性肾脏病患者心血管疾病的病因和进展中起主要作用。由于CKD-MBD主要关注三个类别(骨骼异常、实验室异常和血管钙化),我们通常将异位心血管钙化视为CKD-MBD心脏事件病理生理学中的一个核心危险因素。然而,最近有令人信服的证据表明,除血管钙化外,一些CKD-MBD特异性因素可能也会导致心血管疾病的发生。最值得注意的是成纤维细胞生长因子-23(FGF23),它被认为与心脏重塑独立相关。血管钙化和心脏重塑等心脏疾病进展缓慢是CKD-MBD所致心脏病的特征。相比之下,在CKD-MBD治疗过程中,如使用低钙透析液或拟钙剂时,若发生QT间期延长,可能会诱发致命性心律失常。由致命性心律失常导致的心力衰竭和心源性猝死等致命性心脏事件的突然发生将是CKD-MBD的另一个独特现象。这可能被定义为CKD-MBD特异性心脏综合征。