Platelet hyperactivation is detected in CKD mice possibly due to the high level of serum IS. (A) Scheme for creation of CKD mouse model and AST-120 treatment. (B) Serum IS levels were measured at 8 weeks after left nephrectomy (n = 8). (C) Flow cytometric analysis of P-selectin expression in platelets in response to 2 μg/mL collagen or 0.05 U/mL thrombin (n = 6). (D) Flow cytometric analysis of the concentration of PMPs in whole blood (i). Quantification of the number of PMPs per 1 μL of whole blood (n = 6) (ii). (B-D) Data are mean ± SD. **P < .01 vs sham group; ^#P < .05, ^##P < .01 vs CKD group, ANOVA. (E) Representative immunostaining images of platelet-monocyte aggregates formation in vivo. The peripheral blood cells were labeled with anti-CD14 (red) and anti-CD41 (green), and visualized by confocal microscopy. Scale bar, 10 μm. White arrows indicate platelets associated with monocytes. (F) Flow cytometric analysis of the percentage of platelet-monocyte aggregates in whole blood in vivo (n = 6). (G) Flow cytometric analysis of platelet-induced CD11b expression in platelet-associated monocytes (n = 6). (H) Representative images of thrombus formation on a collagen-coated flow chamber under shear-flow conditions (i). Scale bar, 50 μm. Quantification of the area of platelet adhesion for each group (n = 6) (ii). (F-H) Data are mean ± SD. **P < .01 vs sham group; ^##P < .01 vs CKD group, ANOVA. BSA, bovine serum albumin; MFI, mean fluorescence intensity.