The saturation and concentration of uric acid in the body at 37°C is approximately 420 μmol/L (7 mg/dl), above which hyperuricemia is defined as hyperuricemia. Uric acid is the end product of purine metabolism and is mainly produced by the enzymatic breakdown of nucleic acids and other purine compounds from cellular metabolism and purines from food. There are two main causes of high serum uric acid: increased uric acid production and decreased uric acid excretion, and sometimes both. Increased uric acid production: This includes both high purine dietary intake and increased metabolic production of endogenous purines. 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 defects in renal processing of uric acid and show reduced uric acid excretion, including reduced glomerular filtration rate, increased tubular reabsorption, reduced tubular secretion and uric acid crystalline deposits. Therefore, the exact cause of high serum uric acid needs to be determined by taking into account the patient’s medical history and relevant tests.