The most important biochemical basis of gout is hyperuricemia. Normal adults produce about 750mg of uric acid daily, 80% of which is endogenous and 20% is exogenous, and this uric acid enters the uric acid metabolic pool (about 1200mg). Problems in any of these links can lead to hyperuricemia. Primary gout is mostly hereditary, but only 10% to 20% of people have a family history of gout in clinical practice. Excessive uric acid production accounts for 10% of the causes of primary hyperuricemia. The main causes are defects in purine metabolizing enzymes, hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficiency and hyperactivity of phosphoribosyl pyrophosphate (PRPP) synthase. Primary renal uric acid excretion is reduced in about 90% of primary hyperuricemia. The specific pathogenesis is unclear and may be a polygenic genetic disorder, but organic renal disease should be excluded. 2, secondary gout Refers to a clinical manifestation secondary to other disease processes, and can also be caused by certain drugs. Myeloproliferative diseases such as leukemia, lymphoma, multiple myeloma, erythrocyte count hyperplasia, hemolytic anemia and cancer can lead to accelerated cell proliferation and increased conversion of nucleic acids, resulting in increased production of uric acid. Malignant tumors cause massive cell destruction after radiotherapy of the tumor, and nucleic acid conversion also increases, resulting in increased uric acid production. Renal diseases including chronic glomerulonephritis, pyelonephritis, polycystic kidney, lead poisoning and advanced hypertension cause decreased glomerular filtration function, which can reduce uric acid excretion and lead to increased blood uric acid concentration. Drugs such as thiazide diuretics, furosemide, ethambutol, pyrazinamide, small doses of aspirin and niacin can competitively inhibit renal tubular excretion of uric acid and cause hyperuricemia. In addition, hyperuricemia can also occur in renal transplant patients on long-term immunosuppressants, which may be related to the inhibition of renal tubular excretion of uric acid by immunosuppressants.