Abstract
Cardiovascular mortality increases with decreasing renal function although the cause is yet unknown. Here, we have investigated whether low chronic inflammation in chronic kidney diseases (CKD) could contribute to increased risk for coronary artery diseases (CAD). Thus, a prospective case–control study was conducted in patients with CAD and CKD undergoing coronary artery bypass graft surgery with the aim of detecting differences in cardiovascular outcomes, epicardial adipose tissue volume, and inflammatory marker activity associated with renal dysfunction. Expression of membrane CD14 and CD16, inflammatory cytokines and chemokines, mitogen-activated protein (MAP) kinases and hsa-miR-30a-5p were analyzed in peripheral blood mononuclear cells (PBMCs). Epicardial fat volume and tissue inflammation in perivascular adipose tissue and in the aorta were also studied. In the present study, 151 patients were included, 110 with CAD (51 with CKD) and 41 nonCAD controls (15 with CKD). CKD increased the risk of cardiac surgery–associated acute kidney injury (CSA-AKI) as well as the 30-day mortality after cardiac surgery. Higher counts of CD14++CD16+ monocytes were associated with vascular inflammation, with an increased expression of IL1β, and with CKD in CAD patients. Expression of hsa-miR-30a-5p was correlated with hypertension. We conclude that CKD patients show an increased risk of CSA-AKI and mortality after cardiovascular surgery, associated with the expansion of the CD14++CD16+ subset of proinflammatory monocytes and with IL1β expression. We propose that inflammation associated with CKD may contribute to atherosclerosis (ATH) pathogenesis.
Highlights
Atherosclerotic vascular disease is more common and severe in patients with chronic kidney disease (CKD) and increases their mortality risk [1,2]
The identification of factors linking CKD and coronary artery diseases (CAD) should improve the current understanding of how an impaired kidney function leads to higher cardiovascular risks as well as to identify novel therapeutic targets
We evaluated inflammatory markers in 41 aortic samples (Figure 2 shows a representative sample with the three different degrees of severity in the mononuclear infiltration of the intima used to score the lesions), as well as in 82 samples from epicardial adipose tissue (EAT) and other 58 samples from perivascular adipose tissue (PVAT) (Figure 3 shows the inflammation observed in EAT and PVAT in four different patients)
Summary
Atherosclerotic vascular disease is more common and severe in patients with chronic kidney disease (CKD) and increases their mortality risk [1,2]. Monocytes are a heterogeneous population with a differential functional role [10] and human monocytes have been classified based on their profiles of CD14 (LPS co-receptor) and CD16 (low-affinity FCγ receptor type III) expression into three subtypes: “classical” CD14++/CD16−, “intermediates” CD14+CD16++, and “non-classical” CD14++/CD16+ monocytes [11]. In this sense, it is important to notice that the definition of monocyte subpopulations is challenging since expression of the CD16 marker is continuous, and there is as yet no consensus in the demarcation of the different monocyte subsets that could facilitate the development of functional studies [12,13]. All these data suggest that the different monocyte subpopulations might have different biological functions in ATH progression
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