Discussion
In this study, we have investigated APV, EFT, and CIMT levels in CKD stages. The key findings of this study are as follows. First, stage IV-V patients had the lowest APV and highest EFT and CIMT. Second, GFR was correlated negatively with APV and positively with EFT and CIMT. Third, APV was significantly and negatively correlated with EFT and CIMT in CKD patients. Last but not least, APV, EFT, and CIMT were independently associated with GFR levels in CKD patients.
APV is an aortic stiffness parameter that can be measured during a routine echocardiographic examination. APV is correlated with aortic strain and aortic distensibility in patients with CAD (19). Arterial stiffness is one of the early signs of cardiovascular dysfunction in CKD patients (20). A decrease in propagation velocity can be observed with arterial stiffening in CKD patients. PWV, a marker of arterial stiffness, is an independent predictor of all-cause mortality and cardiovascular mortality in end-stage renal failure patients (21). It was reported that GFR is negatively correlated with arterial stiffness, and increased PWV could predict the presence of CKD (17). Reduced arterial stiffness improved life expectancy in end-stage renal failure patients regardless of blood pressure status (22). In this study, we showed that stage IV-V patients had the lowest APV. This result is compatible with the work by Wang et al., who found that arterial stiffness gradually increased over time as CKD progress. Moreover, our finding shows that arterial stiffness increases gradually as GFR decreases. APV was significantly and positively correlated with GFR levels that show the potential damage of both structure and function of large vessels in patients with CKD. Due to the negative correlation among the APV, EFT, and CIMT levels in CKD patients, APV can be considered as a surrogate marker in subclinical atherosclerosis.
EAT contributes to cardiac function through paracrine and vasocrine secretion of pro-inflammatory and pro-atherogenic cytokines into the myocardial structures. EAT has its protective effects in healthy people, such as mechanical protection, regulation of coronary flow, and energy supplementation of fatty acids. The pathological increase in EFT is associated with increased cardiovascular disease in CKD patients (9). The reason for the increase in EFT is not fully understood in CKD patients. It has been suggested that increased inflammation plays a role in the increase of EFT in these patients (23). Aydın et al. reported that hemodialysis was an independent predictor of increased EFT (24). Patients with essential HT and microalbuminuria had higher EFT compared to HT patients with normoalbuminuria (25). Another study proposed that EFT was an independent predictor of albuminuria in type 2 DM patients (26). Cordeiro et al. evaluated the EFT in 227 non-dialysis CKD patients and reported that EFT correlated with cardiovascular disease severity. Moreover, the authors found that increased EFT was related to poor cardiovascular prognosis (12). A meta-analysis, including the results of 17 studies, suggested that EFT and epicardial fatty volume were increased in CKD patients compared to the control group subjects (27). Sheng et al. evaluated epicardial fatty volume by computed tomography in 120 CKD patients and 30 healthy subjects. They found that stage IV-V patients had higher epicardial fatty volumes compared to the controls (28). Despite this, Ozkurt et al. showed that EFT was similar in CKD patients and control subjects (29). In this study, we found that stage IV-V patients had the highest EFT. This result is supported by a meta-analysis by Song et al. (27). Besides, we reported that EFT was correlated negatively with APV. The result is similar to work done by Turan et al. (30).
CIMT is considered a marker of subclinical atherosclerosis. The increased CIMT has been previously reported in CKD patients. The increased CIMT was associated with low-grade systemic inflammation in CKD patients (31). Higher CIMT was associated with progressively decreasing GFR. Moreover, in CKD patients, GFR could predict the increase in CIMT (16). CIMT is associated with a high mortality rate in CKD patients (32). A previous study showed that CIMT was significantly higher in hemodialysis patients compared to the control subjects (24). CIMT is independently associated with microalbuminuria in type 2 DM patients (33). Patel et al. investigated CIMT in 62 CKD patients and 50 controls. They found that CIMT was significantly higher in CKD patients compared to the controls. Furthermore, the authors showed that dialysis patients had higher CIMT compared to stage III and V (31). Another study indicated that HT patients with CKD had significantly higher CIMT compared to HT patients without CKD (17). In contrast, Margekar et al. found no significant differences in CIMT in different stages of CKD (34). In this study, we showed that CIMT is significantly and negatively correlated with GFR. This finding is consistent with previous findings in the literature (16). Similar to the results of this study, Patel et al. observed the highest CIMT in stage V patients (31).