Blood 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 at 37°C is about 420 μmol/L (7 mg/dl), above which hyperuricemia is considered. It is possible that the increase in uric acid is related to the kidneys. There are two main types of causes of high blood uric acid: increased uric acid production and decreased uric acid excretion, and sometimes both of them coexist. First, increased uric acid production: mainly includes 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 mainly 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 and other factors. Second, blood uric acid excretion is reduced: 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 bile duct. About 90% of patients with persistent hyperuricemia have a defect in renal processing of uric acid, which is manifested by reduced uric acid excretion, including reduced glomerular filtration rate, increased tubular reabsorption, reduced tubular secretion and urate crystalline deposition. Therefore, if hyperuricemia is caused by decreased uric acid excretion, it may be a kidney problem; if hyperuricemia is caused by increased uric acid production, it is not a kidney problem. However, it is worth noting that long-term hyperuricemia can eventually cause kidney lesions as well.