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. Hyperuricemia (HUA) is generally considered to be when fasting blood uric acid levels are higher than 420 μmol/L in men and 357 μmol/L in women on two non-same days under a normal purine diet, which is called hyperuricemia. 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. There are two main types of causes of high 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 uric acid production from endogenous purine metabolism. Food-induced uric acid production is proportional to the purine content of the food, and purine-rich foods include mainly animal offal and seafood. The increase of endogenous purine metabolism is mainly related to the abnormal 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 the function of the kidneys in handling uric acid and show reduced uric acid excretion, including reduced glomerular filtration rate, increased tubular reabsorption, reduced tubular secretion and uric acid crystals deposition. Therefore, high uric acid is mainly caused by the increase of uric acid production and the decrease of uric acid excretion, but the specific cause needs to be combined with the patient’s symptoms and related tests to confirm the diagnosis.