Inflammation is central to chronic kidney disease (CKD) pathogenesis and vascular outcomes, but the exact players remain unidentified. Since low density granulocytes (LDGs) are emerging mediators in inflammatory conditions, we aimed to evaluate whether LDGs may be altered in CKD and related to clinical outcomes as biomarkers. To his end, LDGs subsets were measured in peripheral blood by flow cytometry and confocal microscopy in 33 CKD patients undergoing peritoneal dialysis and 15 healthy controls (HC). Analyses were replicated in an additional cohort. DEF3 (marker of early granulopoiesis) gene expression on PBMCs was quantified by qPCR. Total CD15 LDGs and both CD14CD16 and CD14CD16 subsets were expanded in CKD. The relative frequency of the CD14CD16 subpopulation was higher among the CD15 pool in CKD. This alteration was stable over-time. The increased CD14CD16CD15 paralleled Kauppila scores and DEF3 expression, whereas no association was found with CD14CD16 CD15. Both subsets differed in their CD11b, CD10, CD35, CD31, CD62L, IFNAR1 and CD68 expression, FSC/SSC features and nuclear morphology, pointing to different origins and maturation status. In conclusion, LDGs were expanded in CKD showing a skewed distribution towards a CD14CD16CD15 enrichment, in association with vascular calcification. DEF3 expression in PBMC can be a marker of LDG expansion.