Uric acid in the body originates 80% from endogenous purine metabolism and 20% from purine or nucleic acid rich protein foods. The level of blood uric acid is influenced by multiple factors such as race, diet, region, age, and body surface area. 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 as well as purines from food. The saturation and concentration of uric acid in the body at 37℃ is about 420μmol/L (7mg/dl), above this concentration is hyperuricemia; clinically, it is generally considered that hyperuricemia (HUA) refers to two fasting blood uric acid levels higher than 420μmol/L in men and 357μmol/L in women on non-same day under normal purine diet status, which is called hyperuricemia. There are two main types of causes of hyperuricemia: increased uric acid production and decreased uric acid excretion, often both of which coexist. Increased uric acid production: This includes both high purine dietary intake and increased uric acid production due to abnormal 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 in the body is mainly related to the abnormal synthesis and breakdown 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 impaired renal function due to deposition of urate crystals in the kidney. Therefore, high uric acid is mainly caused by two main reasons: increased uric acid production and reduced uric acid excretion.