With the improvement of living standards, the incidence of gout and hyperuricemia in China is gradually becoming younger, and the number of people suffering from the disease is also rising steeply. It is estimated that the number of people suffering from hyperuricemia in China is 120 million, of which gout patients account for about 10%. Previously, it was thought that long-term hyperuricemia only caused gouty arthritis. However, more and more studies have shown that hyperuricemia is closely related to chronic kidney disease, hypertension, left ventricular hypertrophy, insulin resistance, obesity, hyperlipidemia, abnormal glucose tolerance, etc. It is an important factor that aggravates atherosclerosis and promotes the occurrence and progress of cardiovascular and cerebrovascular diseases, and also induces and aggravates kidney damage. As early as the 1960s, it was confirmed that about 30% to 50% of patients with gout had renal insufficiency and 75% to 95% had interstitial fibrosis and glomerulosclerosis, and Iseki’s 7-year follow-up of 48,177 Japanese adults confirmed that the risk of end-stage renal disease increased 4-fold and 9-fold in men and women with hyperuricemia ≥420 μmol/L and 360 μmol/L, respectively. 9-fold. A retrospective cohort study of 1285 Japanese men aged 40 years or older followed for up to 18 years with a mean follow-up time of 95.2±66.7 months suggested that patients with blood uric acid levels >420 μmol/L had a significantly increased risk of new-onset chronic kidney disease by approximately 3-fold. The incidence of intrarenal arteriopathy was significantly higher in patients with IgA nephropathy with blood uric acid levels >360 μmol/L. The incidence of renal arteriopathy in patients with blood uric acid > 480 μmol/L was 87.4% (23% in the former) compared with blood uric acid ≤ 360 μmol/L. In addition, elevated blood uric acid is also strongly associated with the incidence of diabetic nephropathy and the survival rate of renal transplantation. Recent meta-analyses have shown that the available epidemiological and pilot studies of hyperuricemia and blood uric acid, as well as a small number of small sample interventional studies, indicate that uric acid plays an important role in the development of chronic kidney disease and deterioration of renal function. In patients with chronic kidney disease with blood uric acid levels >420 μmol/ in men and >360 μmol/ in women, it is reasonable to initiate uric acid-lowering therapy. For patients of Asian descent, the threshold for treatment may be even lower! Studies have confirmed that when blood uric acid is elevated, it can cause a series of pathophysiological changes in the kidney. High uric acid not only activates renin-angiotensin activity, but also raises plasma renin levels and leads to systemic hypertension and release of inflammatory mediators through angiotensin II, producing a “triple high” in the glomerulus; in addition, uric acid can impair endothelial cell function and affect prostaglandin production. Currently, common clinical drugs include xanthine oxidase inhibitors (allopurinol, febuxostat), which inhibit uric acid synthesis, and drugs that increase uric acid excretion by inhibiting renal tubular uric acid reabsorption (benzbromarone, propofol). Treatment options should be chosen according to the staging of hyperuricemia and the needs of the disease. It should be noted that allopurinol carries the risk of serious hypersensitivity reactions such as bone marrow suppression, leukopenia and thrombocytopenia and even exfoliative dermatitis. Febuxostat is also associated with cardiovascular risks such as hepatic dysfunction and atrioventricular block. Benzbromarone is indicated for patients with mild to moderate renal insufficiency with Ccr >20 ml/min or more, but it also carries a few risks such as allergic and gastrointestinal reactions. In addition to pharmacological treatment, dietary treatment of hyperuricemia is also very important. For patients with hyperuricemia, we recommend to do no broth; blanch meat before making it; eat less seafood, shellfish, animal offal, fatty meat, dried foods (mushrooms, nori, kelp, etc.), beans, nuts and other high purine foods; no alcohol, less honey and sweet drinks; patients with normal urine output and no water overload can drink more water appropriately.