Background There is a high incidence of hyperuricemia among residents in southern coastal areas under high temperature and high humidity environment.

Objective To establish an animal model of hyperuricemia caused by high temperature and high humidity environment, and explore the pathological changes in kidney, liver and ankle joints.

Methods A total of 30 SPF-SD male rats were divided into control group (CON, n=6), potassium oxonate group (PO, n=6), high purine diet group (HPD, n=6), high temperature-humidity group (HT, n=6), and compound factor group (CF, n=6). The rats from CON group were only given 0.5% sodium carboxymethyl cellulose solution by gavage. PO group was gavaged with 250mg/kg potassium oxonate suspension, while HPD group was gavaged with 250 mg/kg potassium oxonate suspension and fed with 20% yeast feed. On the basis of the above intervention modeling methods for the PO group and the HPD group, HT group and CF group were irradiated in a special constant temperature incubator with a temperature of (37±0.5)℃ and a relative humidity of 80%±1% for 1 h/d. The experiment lasted for 12 continuous weeks, at the time of 0 week, 6^th week and 12^th week, all rats were fasted for at least 12 h before collecting blood samples so as to test their serum uric acid level. Three rats from each group were anesthetized to collect their renal, heart, liver and ankle tissues after modeling for 6 weeks and 12 weeks respectively.

Results The serum uric acid levels of CF group, HT group, HPD group PO group were significantly higher than that of CON group (P < 0.05), and that of HT group was higher than PO group (P < 0.05), CF group was higher than HPD group (P < 0.05). In this experiment, renal tissue morphology in the PO group and HPD group showed tubular dilation, whereas the HT and CF groups exhibited marked swelling of proximal tubular epithelial cells, narrowing of the tubular lumen, and partial tubular lumens with significant inflammatory infiltration. In addition, the CF group also presented partial atrophy of renal tubular epithelial cells. Under light microscopy, mild dilation of hepatic sinusoids was observed in the PO and HPD groups, while hepatocytes were swollen and hepatic sinusoids narrowed in the HT and CF groups. In the CF group, myocardial fibers were slightly disarranged in arrangement, and the structure of the articular cartilage layer at the ankle joint appeared uneven; no obvious abnormalities were found in the remaining tissues. At 6 weeks after modeling, urate crystal deposition was detected in the HPD, HT, and CF groups, with the most severe deposition observed in the CF group. By 12 weeks, crystal deposition in all three groups (HPD, HT, and CF) had decreased to some extent.

Conclusion Hyperuricemia rat model prepared by 12-week high-temperature-humidity environment treatment presents extensive changes in the morphology of kidney, liver, heart and ankle joints.