Coronary artery disease in chronic kidney disease is characterized by endothelial dysfunction, decreased coronary flow reserve, and severe vascular calcification, complicating diagnosis and treatment.
This review highlights the complex pathophysiology of CAD in CKD, emphasizing the roles of endothelial dysfunction, decreased coronary flow reserve, and severe vascular calcification, which complicate revascularization strategies.
Patients with chronic kidney disease (CKD) commonly experience cardiovascular disease (CVD), and a major cause of death in these patients is CVD. Therefore, the prevention of CVD progression is very crucial in patients with CKD. Recently, this relationship between CKD and CVD has increasingly been examined, and a concept termed "cardiorenal syndrome" has been advocated. Coronary artery disease (CAD) and myocardial injury are crucial factors that contribute to the occurrence of CVD. The initial step CAD is endothelial dysfunction that can be detected as a decrease in the coronary flow reserve (CFR). The previous studies have reported that decreased CFR is significantly correlated to coronary events and mortality. Furthermore, CFR reduces with a decline in the kidney function. Another important presentation of CAD is coronary artery calcification. Vascular calcification is a crucial pathophysiological state, particularly in patients with CKD, and it affects the stability of coronary atherosclerotic plaque. In CKD, not only the traditional risk factors but also CKD-related non-traditional risk factors play key roles in CVD progression. Therefore, the mechanisms responsible for CVD progression are very complex; however, their clarification is crucial to improve the prognosis in patients with CKD.
Fujii et al. (2019) conducted a review in Coronary artery disease in chronic kidney disease. Coronary artery disease in chronic kidney disease is characterized by endothelial dysfunction, decreased coronary flow reserve, and severe vascular calcification, complicating diagnosis and treatment.