Generally speaking, high blood uric acid is caused by two main reasons: increased uric acid production and decreased uric acid excretion, which should be further determined by the patient’s medical history and related tests. 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. The saturation and concentration of uric acid in the body at 37°C is about 420 μmol/L (7 mg/dl), above which hyperuricemia can be considered. In clinical practice, it is generally considered that hyperuricemia (HUA) is defined as two fasting blood uric acid levels higher than 420 μmol/L in men and 357 μmol/L in women on non-same day under normal purine diet status. Increased uric acid production: It mainly includes both high purine diet intake and increased endogenous purine metabolism production. Food-induced uric acid production is proportional to the purine content of food. Purine-rich foods mainly include animal offal (liver, kidney, heart, brain, etc.), seafood (wind-tailed fish, sardines, fish eggs, small shrimp, etc.), and thick meat soup. Increased endogenous purine metabolism production in the body is mainly related to factors such as abnormal synthesis and decomposition of purines. 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 intestine 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 should promptly seek medical attention to find the specific cause of the disease to avoid delay.