Background: The risk of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) is estimated to be far greater than that in the general population. Adropin regulates endothelial function and may play a role in the pathogenesis of CVD. Angiotensin-converting enzyme inhibitor (ACEI) treatment was reported to have a protective effect on both renal and cardiovascular function. This study investigated whether adropin is associated with renal and cardiovascular outcomes after using ACEI treatment in CKD rats. Methods: In 2021, in Zagazig, Egypt, rats were assigned to: GI, control group (n=8); GII, CKD group (n=8), and GIII, CKD+captopril group (n=8), in which CKD rats received 100 mg/Kg/day captopril orally. Adropin levels, renal function, blood pressure, and various CVD risk factors were measured. Renal, cardiac, and aortic tissues were examined histologically and immunohistochemically to detect the expression of vascular endothelial growth factor receptor-2 (VEGFR-2). To analyze data, ANOVA and Pearson's correlation tests were used (SPSS version 18, P<0.05 is significant). Results: Adropin was significantly lower in GII than in GI and GIII (P<0.001). Adropin in GII and GIII was negatively correlated with atherogenic index (P=0.019 and P=0.001, respectively), atherogenic co-efficient (P=0.012 and P=0.013, respectively), troponin I (P=0.021 and P=0.043, respectively), and nitric oxide (P=0.025 and P=0.038, respectively). VEGFR-2 expression decreased in GII and was elevated in GIII (P<0.001). Conclusion: Adropin levels were significantly correlated with most CVD risk factors in CKD and captopril-treated CKD rats, indicating a role for adropin in the pathogenesis of CVD in CKD. It also refers to its implication in the ameliorative effect of ACEI treatment, possibly by affecting VEGFR-2 and nitric oxide release.