*2.5. Inflammation*

CKD can be seen as a state of increased systemic inflammation with various cytokines being among the recognized uremic toxins. The Chronic Renal Insu fficiency Cohort Study (CRIC) study found that elevated plasma levels of high-sensitivity C-reactive protein (hs-CRP) and IL-6 were associated with LVH and systolic dysfunction in CKD patients [41]. Freise et al. stated that, amongs<sup>t</sup> others, inflammatory processes involving tumor necrosis factor (TNF) and IL-10 impact pathobiological responses in arteries from children with CKD, and are thus associated with tissue remodeling and cardiovascular disease [42]. Furthermore, CKD patients develop endotoxemia, characterized by elevated levels of endotoxin, IL-6, CRP and lipopolysaccharide-binding protein (LBP), which contributes to chronic inflammation and has been associated with higher left-ventricular mass index (LVMI) and subsequently left-ventricular dysfunction [43]. Most of the soluble factors mentioned here are described as being secreted by cells of the heart (cardiomyocytes, endothelial cells, fibroblasts, VSMCs and pericytes) but also resident immune cells (e.g., macrophages, dendritic cells) and/or circulating cells might contribute to this. Thus, the contribution of inflammatory cells to the described mechanisms cannot be excluded.
