Uric acid is the end product of purine metabolism and is mainly produced by the enzymatic breakdown of nucleic acids and other purine analogues from cellular metabolism and purines from food. The saturation and concentration of uric acid in the body is about 420 μmol/L (7 mg/dl) at 37°C. Above this concentration, hyperuricemia is defined as hyperuricemia. There are two main types of causes of high uric acid: increased uric acid production and decreased uric acid excretion, and sometimes both of them coexist. Increased uric acid production: This includes both high purine dietary intake and increased endogenous purine metabolism. Food-induced uric acid production is proportional to the purine content of food, and purine-rich foods include animal liver, kidney, anchovies, etc. The increase of endogenous purine metabolism in the body is mainly related to the synthesis and decomposition of purine. Decreased uric acid excretion: About 2/3 of uric acid is excreted through the kidneys, and the remaining 1/3 is excreted through extrarenal pathways such as the intestinal tract and biliary tract. About 90% of patients with persistent hyperuricemia have a defect in renal processing of uric acid and show reduced uric acid excretion, including reduced glomerular filtration rate, increased tubular reabsorption, reduced tubular secretion and urate crystallization. In general, high uric acid is mainly caused by the increase of uric acid production and the decrease of uric acid excretion, but the exact cause should be clarified by the patient’s medical history and related examination.