*2.1. Left-Ventricular Hypertrophy in CKD*

LVH is an independent predictor of cardiac death in dialysis patients. LVH can occur early in the course of CKD, even when the glomerular filtration rate (GFR) is still normal [16]. Once GFR is reduced, myocytes enlarge and cardiomyocytes expand, leading to LVH [17]. Cardiomyocytes are the major cell type, comprising about 70–85% of the total volume. They generate contractility by cyclic calcium fluxes [17,18]. Fibroblasts secrete collagen precursors and matrix metalloproteinases (MMPs) and thereby actively remodel the ECM [17–19]. The ECM embeds the myocytes and non-myocytes. Collagen is the most abundant protein here [19]. These structural changes are closely related to a functional impairment of the left ventricle causing diastolic dysfunction [20] while systolic function may, at least initially, remain normal [21]. LVH can be a consequence of increased preload due to hypervolemia or increased afterload due to increased peripheral resistance or hypertension, which are both very common in CKD. Further factors involved in the pathogenesis of LVH might be high cardiac output due to anemia or large arteriovenous fistulas for dialysis access [18,21].
