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.