What are the risk factors for developing hyperuricemia?

  Uric acid is a product of purine metabolism in the body. There are two sources of human purine, endogenous to its own synthesis or nucleic acid degradation (about 600mg/d), which accounts for about 80% of the total uric acid in the body, and exogenous to the intake of purine diet (about 100mg/d), which accounts for about 20% of the total uric acid in the body. In the normal state, the uric acid pool in the body is 1200mg, the blood urate saturation is 6.7mg/dl, the daily production of uric acid is about 750mg, excretion is about 800-1000mg, 30% is excreted from the intestinal tract and biliary tract, 70% is excreted by the kidneys. The daily production and excretion of uric acid in the human body is basically in dynamic balance, and any factor that affects the production and/or excretion of uric acid in the blood can lead to an increase in blood uric acid levels. The kidney is an important organ for uric acid excretion, and a 5-25% decrease in renal creatinine clearance can lead to hyperuricemia (HUA).  Hyperuricemia is associated with age, gender, regional distribution, race, genetics, and social status. Hyperuricemia is more likely to occur with increasing age, in men, in first-degree relatives with a history of hyperuricemia, in people with sedentary lifestyles and high social status, and in patients with cardiovascular risk factors and renal insufficiency.  Consumption of high purine foods such as meat, seafood, animal offal, thick broths, etc., alcohol consumption (beer, liquor) and strenuous physical exercise can increase blood uric acid. The prolonged application of certain drugs can lead to increased blood uric acid, such as thiazide diuretics, compound antihypertensive tablets, pyrazinamide, nifedipine, propranolol, etc. all prevent uric acid excretion.