Foot pain caused by high uric acid is usually caused by uric acid crystals depositing in the joints, leading to gouty arthritis. The main reasons include abnormal purine metabolism, high purine diet, reduced kidney excretion, obesity, and genetic factors.

1. Abnormal purine metabolism:
Disruption of purine metabolism in the human body can lead to excessive production of uric acid. After purine decomposition, uric acid is produced. When the enzyme system functions abnormally, the synthesis rate of uric acid exceeds the excretion capacity, and the concentration of uric acid in the blood increases, forming a supersaturated state, and ultimately depositing needle shaped crystals in the joint cavity.
2. High purine diet:
Long term intake of high purine foods such as animal organs, seafood, and concentrated meat soup can significantly increase the source of exogenous uric acid. Every 100 grams of pig liver contains about 300 milligrams of purine, far exceeding the recommended daily intake. Continuous high load intake may trigger acute gout attacks. 3. Reduced renal excretion: Approximately 70% of uric acid is excreted through the kidneys. Renal dysfunction or certain medications such as diuretics can inhibit the secretion of uric acid by the renal tubules. When the glomerular filtration rate is below 60ml/min, the efficiency of uric acid excretion significantly decreases, and the blood uric acid level is prone to exceed the saturation critical point of 420 μ mol/L. 4. Obesity factors: Inflammatory factors secreted by adipose tissue can interfere with uric acid metabolism. For every 1kg/m ² increase in body mass index, blood uric acid levels rise by approximately 16 μ mol/L. accumulation of visceral fat can also lead to insulin resistance, further reducing the kidney's ability to clear uric acid.
5. Genetic susceptibility: About 30% of gout patients have genetic variations such as SLC2A9 or ABCG2, which encode transporters involved in uric acid excretion. People with a family history may experience joint symptoms earlier, even if their blood uric acid levels are slightly elevated, and the age of onset may be 10-15 years earlier.

To control uric acid, it is necessary to limit daily purine intake to below 200mg, avoid drinking alcohol and sugary drinks, and drink more than 2000ml of water per day to promote excretion. It is recommended to choose low-fat dairy products, eggs, vegetables and other low purine foods, and regularly engage in low impact exercises such as swimming and cycling. During acute attacks, joint weight-bearing should be reduced, and blood uric acid levels should be continuously monitored during the intermission period. Maintaining a value below 300 μ mol/L can significantly reduce the risk of recurrence. Patients with hypertension or diabetes should pay special attention to drug selection and avoid using antihypertensive drugs that affect uric acid metabolism.

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