A paradoxically positive adiponectin-endothelial activation relationship was also documented in white patients with RA. The potential role of RBP4 in atherogenesis and CVD risk stratification in RA has, to our knowledge, not been investigated. In the present study, we measured RBP4 concentrations, surrogate markers of enhanced early atherogenesis comprising E-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and monocyte chemoattractant protein-1, and common carotid artery intima-media thickness and carotid artery plaque by ultrasound in both black and white patients with RA. We examined the independent relationships of RBP4 concentrations with cardiometabolic risk, endothelial activation and carotid atherosclerosis. In this RA study, adiposity was not associated with RBP4 concentrations. However, obesity adversely influenced the impact of this adipokine on atherosclerosis. Indeed, RBP4 concentrations were independently related to increased carotid Axitinib atherosclerosis only in patients with overall and abdominal obesity. Further, although RBP4 concentrations were lower in black compared to white patients, they were associated with atherosclerosis in the former but not the latter. This was possibly due to the far larger prevalence of excess adiposity in black compared to white patients. Consideration of RBP4 concentrations may improve cardiovascular risk stratification in RA. Paradoxical adipokine – CVD risk associations as we found between RBP4 concentrations and metabolic risk and endothelial activation, were previously reported. Such relations are thought to represent a compensatory change in adipokine production in the presence of chronic vascular disease and aimed at reducing metabolic risk. However, we found that the presence of plaque did not influence the impact of RBP4 concentrations on cardiovascular risk. By contrast, the inverse RBP4 – CVD risk associations were mostly reproduced only in patients with adverse traditional or nontraditional cardiovascular risk profiles. Our cross-sectional study design precludes drawing inferences on the direction of causality. Additionally, our findings on the associations of RBP4 concentrations with metabolic risk factors and endothelial activation differ and in fact contrast to those previously reported in non-RA subjects. Therefore, these relations need further study. RBP4 induces insulin resistance. We did not directly assess this metabolic risk factor. RBP4 concentrations were nonetheless not associated with the triacylglycerols-HDL cholesterol and leptin-adiponectin ratios, which are surrogate markers of insulin resistance. Future studies on the potential impact of RBP4 on metabolic risk in RA should include markers of insulin resistance such as the homeostasis model assessment of insulin resistance. Our finding of lower RBP4 concentrations in black compared to white patients with RA is congruent with an earlier investigation that showed disparities in RBP4 gene polymorphisms amongst black and white Americans.