OBJECTIVES/GOALS: Platelets interact with leukocytes in the circulation to modulate inflammation in chronic diseases. In previous clinical study, we showed that platelet leukocyte interaction is reduced in the circulation of patients with CKD. Preclinical studies are needed to show whether these findings are a precursor to or a result of CKD. METHODS/STUDY POPULATION: We used mouse models (wild type and platelet-defect) and induced CKD with intraperitoneal cisplatin injections. We measured platelet leukocyte interactions before and after CKD induction in the two models. RESULTS/ANTICIPATED RESULTS: We found platelet-leukocyte interaction to reduce after CKD induction in both wild type and platelet-defect mice. This coincided with a pro-inflammatory state in these mice, as measured by serum TNFalpha levels. Specifically, pro-inflammatory state was exacerbated in CKD of mice with platelet-defects compared to the wild type. DISCUSSION/SIGNIFICANCE: These findings recapitulate translational findings in human CKD samples and confirm that CKD state results in reduced platelet-leukocyte interactions in the circulation, and this change imparts a pro-inflammatory state in the CKD state.