Chronic kidney disease (CKD) poses a significant global threat, with increased rates of cardiovascular and all-cause mortality. Anemia is common in CKD, and is often associated with the accumulation of uremic toxins in the bloodstream. Previously, we demonstrated that the uremic toxin indoxyl sulfate (IS) has an impact on the regulation of erythropoiesis in both cellular and preclinical CKD models. In this study, on the roles of non-coding RNAs in this toxin/toxic effect, we measured the effect of IS on microRNA expression in the human erythropoietic cell line UT7/EPO, using nanostring technology. We found a significant increase in miR-223 in cells treated with IS. This finding was further validated in human primary CD34+ cells, a more physiological model for human erythropoiesis. Finally, serum levels of miR-223 correlated with representative uremic toxins, including IS, in patients with various stages of CKD, and also with endothelial dysfunction markers, indicating a link with vascular damage. These findings suggest that miR-223 may contribute to the development of anemia in CKD. Further investigation into the involvement of miR-223 in erythropoiesis is needed for a better understanding of the mechanisms underlying anemia in CKD and the potential role of uremic toxins. Ultimately, this may open up new therapeutic possibilities for the management of anemia in CKD.