Background: Hyperuricemia (HUA) is the direct cause of gouty arthritis. The association between cardiometabolic index (CMI) and hyperuricemia remains unclear. This study aimed to examine this association in the middle-aged and elderly Chinese for preventing gouty arthritis at early stage. Method: This study was based on China Health and Retirement Longitudinal Study (CHARLS, survey 2011 and 2015). Four logistic regression models were established. Sensitive analysis including propensity score matching (PSM) and inverse probability of treatment weighting (IPTW), etc. were applied to identify the robustness of the models. Restricted cubic spline (RCS) was adopted to further explore the non-linear relationship between the CMI and hyperuricemia. Moreover, as the HUA was caused by the abnormal elevation of serum uric acid (SUA), Cross-lagged panel model (CLPM) was used to investigate the causal relationship between CMI and SUA. Mediation analysis was used to explore the possible mechanisms about the interference of CMI to HUA. Results: A total of 5,653 participants were enrolled in this study. A positive association between CMI and hyperuricemia was found in both the cross-sectional and longitudinal analysis. In the four logistic regression models of longitudinal analysis, the ORs were 2.09(1.73,2.54), 2.20(1.81,2.68), 2.09(1.71,2.56) and 1.93(1.57,2.36), respectively. Results maintained consistent in the sensitive analysis including PSM and IPTW. Importantly, it still holds in the participants with normal body mass index. Additionally, a non-linear relationship was revealed via RCS (p for non-linearity = 0.037). Further, CLPM demonstrated that higher CMI can directly associated with SUA increasing (standardized beta = 0.06, p < 0.001). Moreover, mediation analysis proved that CRP (beta = 1.22; p < 0.001) and WBC (beta = 0.28; p < 0.010) can mediated the positive association between CMI and hyperuricemia. Conclusion: Elevated CMI is an independent risk factor for hyperuricemia, and associated with the increasing SUA levels in a temporal sequence manner, effects potentially mediated in part by inflammation.