Aims: To study the effects of uric acid on cardiac lesions and its possible mechanism by establishing an early-stage CKD animal model with hyperuricemia. Allopurinol was used to see whether it could reduce cardiac lesions. Methods: The experimental rats were randomly divided into 4 groups (n = 15): Group A (sham-operative group), Group B (CKD group), Group C (CKD with hyperuricemia group), Group D (CKD with hyperuricemia + allopurinol group). After 16 weeks, the rats were sacrificed and blood samples were collected for detection of Scr, SUA, hs-CRP and IL-6. Kidney and heart tissues were pathologically examined. The collagen I of heart tissues was examined by immunohistochemistrical methods. Results: Obvious pathological changes could be observed in Group C. However, compared to Group C, the pathological changes in Group D were lighter. The proportion of collagen I positive area (PCIPA) in Group C was significantly higher than that in Group A, B and D. Univariate analysis showed that the SUA level had a significant positive correlation with PCIPA in myocardium. IL-6 and hs-CRP levels in Group C were significantly higher than in Group A, B and D. Univariate analysis showed that the SUA level had a significant positive correlation with IL-6 and hs-CRP, and PCIPA in myocardium had a significant positive correlation with hs-CRP and IL-6 levels. Conclusions: There were obvious cardiac lesions in early-stage CKD rats with hyperuricemia, and the severity of cardiac lesions was positively related to the level of SUA. Micro-inflammation might be one mechanism causing cardiac lesions. Allopurinol could alleviate cardiac lesions in early-stage CKD rats by lowering the SUA level, which, in turn, could reduce the severity of micro-inflammation.