Objectives: Chronic kidney disease (CKD) is strongly associated with cardiovascular disease and chronic inflammation makes atherosclerosis in the patients with CKD. Renal GLP-1 activity is decreased in the chronic kidney disease, also GLP-1 receptor (GLP-1 R) activation is related with cardiovascular protection. It is not clear that renal GLP-1 R change in CKD with atherosclerosis. We investigated renal GLP-1 activity in the CKD with atherosclerosis. Methods: CKD models was 5/6th nephrectomized, and atherosclerosis was made with balloon. Animals were divided into seven groups: control, CKD 8 weeks (CKD), CKD with DPP-4 inhibitor (CKD-Lina), carotid artery injury (Athero), Athero-Lina, CKD-Athero, CKD-Athero-Lina. DPP-4 inhibitor-treated groups were orally administered 5 mg/kg of linagliptin mixed in water, once daily for beginning the day after 5/6 nephrectomy. Renal cortical GLP-1 R activity was measured via Western blot analysis and immunohistochemistry which were standardized by beta-actin density. Results: Cortical GLP-1R was significantly decreased in CKD and CKD with carotid injury (p<0.01). After linagliptin treatment, GLP-1R was significantly increased in both the CKD and CKD with carotid injury groups (p<0.01) (Fig 1). Western blot of GLP-1R in carotid artery showed decreased expression in carotid injury and CKD with carotid injury (p<0.01). GLP-1R protein levels were significantly increased in both carotid injury and CKD with carotid injury groups after linagliptin treatment (p<0.01) (Fig 2). IHC showed similar results as western blot. Conclusions: DPP-4 inhibitor treated CKD with Atherosclerosis showed increased GLP-1 R in renal cortex and carotid artery. These suggest that GLP-1 R activity may be associated with renal and vascular protective response of atherosclerosis in CKD.