Introduction
Patients with chronic kidney diseases (CKD) have increased morbidity and mortality compared to the general population. Cardiovascular disease (CVD) is the primary cause of mortality and morbidity in CKD patients. Early vascular aging and arterial stiffness are the most specific changes in arteries in CKD patients, and it can also be seen in the early stages of CKD (1). Many reasons have been asserted for decreased vascular compliance and increased arterial stiffness, including activation of the renin-angiotensin system, vascular calcification, and endothelial dysfunction in CKD patients (2).
Arterial stiffness has been recognized as a vascular biomarker, and it describes the arterial pressure response to stroke volume changes (3). Besides, arterial stiffness is also closely related to the propagation velocity of the pressure. Carotid-to-femoral pulse wave velocity (PWV), accepted as a marker of arterial stiffening, is known to be a strong predictor of morbidity and mortality in CKD patients (4). Arterial stiffness is most prominently observed in the aorta and becomes progressively worse as CKD progresses (5). Aortic propagation velocity (APV) reflects the presence of aortic stiffness and is measured with an echocardiographic method. The measurement of APV is based on the propagation velocity of the descending thoracic aorta. Gunes et al. was used the APV to evaluate aortic stiffness in coronary artery disease (CAD) patients and showed that it is related to carotid and coronary atherosclerosis (6).
Epicardial adipose tissue (EAT) is found between the pericardial visceral layer and myocardium. EAT direct contact with the surface of the myocardium and coronary vessels (7). EAT secrets adipocytokines which have cardioprotective effects (8). The pathological increase in EAT correlated with cardiovascular disease risk (9). Many studies proposed that there was a significant relationship between the CKD and epicardial fat thickness (EFT). Previously increased EFT has been noted in hemodialysis patients (10). Increased EFT is accepted as a cardiovascular risk factor in CKD patients. Nakanishi et al. evaluated EAT volume by computed tomography and showed that CKD patients had more EAT compared to patients without CKD (11). Moreover, Increased EFT has been associated with a worse cardiovascular prognosis in CKD patients (12).
The accumulation of lipids in the arterial wall causes thickening of the intima-media layers and atherosclerotic plaque formation (13). Carotid intima-media thickness (CIMT) is accepted as a marker of subclinical atherosclerosis and is associated with the presence of CAD (14). CKD patients could have subclinical atherosclerosis in the arterial wall. The prominence in the carotid artery wall and outward remodeling was reported in CKD patients (15). CIMT is associated with cardiovascular events and mortality in CKD patients (16). Zuo et al. presented that hypertensive patients with CKD had increased CIMT compared to non-CKD hypertensive patients (17). Another study described that there was a negative correlation between CIMT and estimated glomerular filtration rate (GFR) (16).
APV, EFT, and CIMT measurements could provide additional information on assessing renal decline in CKD patients. We hypothesized that APV, EFT, and CIMT might be related to CKD stages. The study aimed to evaluate EFT, AVP, and CIMT in CKD patients and then investigate the association among those parameters.