Objective To provide approaches for modeling the development of anti-hyperuricemia drugs, acute and chronic hyperuricemia animal models were established, and positive drug was applied to verify the curability of these two animal models. Methods The acute hyperuricemia mouse model was established by the intraperitoneal injection of hypoxanthine and subcutaneous injection of oteracil potassium. Allopurinol tablets were administered to the positive group half an hour after the model establishment. Finally, the concentrations of serum uric acid, serum creatinine, and serum urea nitrogen and the activity of liver xanthine oxidase (XOD) were determined 2 h after model establishment. In contrast, adenine and ethambutol dihydrochloride were used to establish the chronic hyperuricemia rat model by gavage. The positive group was administered allopurinol tablets daily. After 21 days, the concentrations of serum uric acid, serum creatinine, and serum urea nitrogen, the activity of XOD, and the histopathological change of kidneys were determined. Results The concentrations of serum uric acid and serum creatinine were significantly elevated (P< 0. 05) in both the acute and the chronic hyperuricemia models. Additionally, serum urea nitrogen and XOD activity were also clearly elevated (P<0. 05), while renal tubule interstitial injury and urate crystallization could be found, the scores of which were significantly increased in the chronic hyperuricemia model. However, the concentration of serum uric acid was decreased after treatment with allopurinol tablets for both acute and chronic hyperuricemia animals; moreover, in the chronic hyperuricemia animals, the concentration of serum creatinine and activity of liver XOD were decreased, while kidney injury and urate crystallization were also improved. Conclusions The approaches established in this study are suitable for creating acute and chronic hyperuricemia animal models, and can be used for drug pharmacodynamic observation.