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Those subjects who had CD14++CD16+ monocyte counts higher than the median in conjunction with higher CRP levels had the worst outcomes (Online Fig. S1D) in Kaplan-Meier analysis (p Tenofovir ic50 of a distinct monocyte subset has been discussed as a promising therapeutic avenue in atherosclerosis (17). This notion is backed by the successful application of cell-targeted therapy in other fields of medicine, such as the introduction of rituximab in patients with lymphoma (18). Unfortunately, advances in understanding of murine atherosclerosis are not paralleled by a better grasp of human pathology, given that the potential monocyte target subpopulation in atherosclerosis has not been convincingly identified yet. So far, most information derives from few cross-sectional studies: in a heterogenous cohort of 308 subjects, a shift toward CD16-positive monocytes was associated with the presence of coronary artery disease (19). Later, small cross-sectional studies linked high counts of CD16-positive monocytes with the presence of vulnerable atherosclerotic plaques in patients with stable angina pectoris (20) and with fibrous cap thickness in patients with unstable angina pectoris (21). Sitaxentan Of note, none of these studies distinguished intermediate CD14++CD16+ monocytes from nonclassical CD14+CD16++ monocytes (as discussed in detail previously [22?and?23]). Consequently, so far, the respective roles of CD14++CD16+ and CD14+CD16++ monocytes in human atherosclerosis have not been fully discerned. Against this background, selleckchem large prospective studies of monocyte subsets and cardiovascular outcomes have been demanded recently (17). We previously set out to analyze the relationship between subset-specific monocyte counts and adverse cardiovascular outcomes in selected patient groups. Initially, we focused our analysis on patients with CKD receiving dialysis treatment (10, 24?and?25), reasoning that this highest cardiovascular risk group would allow us to gather information in a limited sample size because of the high event rate. This allowed us to demonstrate CD14++CD16+ monocytes to be independent predictors of cardiovascular events in dialysis patients (10). However, a drawback of this approach was the observed strong shift in monocyte subsets toward CD16-positive cells compared with healthy controls (10), precluding a translation of these results to non-CKD populations. Next we prospectively analyzed monocyte heterogeneity in subjects with earlier stages of CKD not requiring dialysis. At baseline, these patients had CD14++CD16+ cell counts between those of subjects with preserved renal function and those of patients with CKD receiving dialysis.