A large number of basic and clinical studies have shown that HUA is an independent risk factor for metabolic diseases (diabetes, metabolic syndrome, dyslipidemia, etc.), chronic kidney disease, cardiovascular disease, stroke and other diseases, and is inseparable from gout. At present, there is no consensus at home and abroad on whether there is a need for treatment of asymptomatic HUA and the determination of treatment standards. ”The Consensus provides a comprehensive and systematic description of the issues related to hyperuricemia from the following parts: (1) epidemiology and hazards of hyperuricemia (HUA); (2) diagnostic and typing criteria of HUA; (3) prevention of HUA; (4) control target and treatment starting point of blood uric acid in HUA patients; (5) treatment of HUA. Treatment of HUA. As mentioned above, HUA is significantly correlated with metabolic syndrome and its components (diabetes and insulin resistance, obesity, hyperlipidemia, hypertension), and HUA is an independent risk factor for the development of type 2 diabetes; multicenter, large-sample systematic review and Meta-analysis and several prospective cohort studies found that HUA is significantly correlated with increased prevalence and risk of death from coronary heart disease. HUA was also an independent risk factor for the development of heart failure and ischemic stroke and death. In addition, with the increase of blood uric acid (SUA), the prevalence of chronic kidney disease and diabetic nephropathy increases significantly, while the survival rate decreases significantly; SUA is also a strong predictor of acute and chronic renal failure, while elevated SUA is the most important biochemical basis and the most direct cause of gout, and HUA is closely related to the occurrence and recurrent attacks of gout, as well as joint destruction and impaired renal function. At present, the international diagnosis of HUA is defined as: under normal purine diet. Clinical studies have shown that 90% of primary HUA is of poor renal uric acid excretion type. In the prevention of HUA, attention should be paid to HUA susceptible groups such as advanced age, men, obesity, history of gout in first-degree relatives, reducing high purine diet intake, appropriately alkalizing urine, avoiding long-term use of some drugs that affect blood uric acid level such as low-dose aspirin and tab diuretics and thiazide diuretics, and performing blood uric acid tests in patients with multiple cardiovascular and metabolic diseases associated with HUA for early detection of Regarding the control target and treatment starting point of blood uric acid in HUA patients, the Consensus recommends that for patients with hyperuricemia combined with cardiovascular risk factors and cardiovascular and metabolic diseases, if the SUA is >420 μmol/L in men and >360 μmol/L in women, life coaching and drug lowering treatment should be carried out at the same time. For patients with gout attacks, long-term control of SUA below 300 μmol/L is required to prevent recurrent attacks. For the treatment of HUA, patients should be encouraged to pay attention to lifestyle changes (including healthy diet, smoking and alcohol cessation, adherence to exercise and weight control) and actively carry out patient medical education to improve patients’ awareness of disease prevention and treatment and improve treatment compliance. Since there is a direct causal relationship between gout and HUA, the treatment of HUA is the key to the treatment of gout. Therefore, the Consensus has formulated the “Gout Treatment Pathway” and “HUA Treatment Pathway” to provide reference and guidance for clinical treatment. Regarding the choice of uric acid-lowering drugs, the drugs currently used in clinical practice mainly include benzbromarone and probenecid, which increase uric acid excretion, and allopurinol, which inhibits uric acid synthesis and xanthine oxidase inhibitors. The mechanism of action of benzbromarone is to inhibit the active reabsorption of urate in the renal tubules and increase the excretion of urate to reduce blood uric acid. Long-term use of benzbromarone has no effect on renal function and can be used in patients with renal insufficiency with Ccr>20ml/min. Clinical studies have confirmed that since more than 90% of HUA is due to reduced uric acid excretion, pro-uric acid excretory drugs should be more widely used. Allopurinol should be started at low doses and gradually increased. The dose should be reduced in patients with renal insufficiency. Common hypersensitivity reactions to allopurinol should be monitored closely at the time of application, occurring mainly within the first few months of use, most commonly with exfoliative dermatitis. There is a close correlation between this adverse reaction and leukocyte antigen (HLA)-B*5801, and the risk of hypersensitivity reactions is greater in Chinese Han Chinese who are 6-8% positive for this allele than in whites (only 2%). Genetic testing is recommended when available, and is prohibited in patients with positive results. Drugs that have been marketed abroad include: non-purine xanthine oxidase selective inhibitors such as febuxostat, which are currently considered suitable for the treatment of patients with gout in the chronic phase and are not recommended for the treatment of patients with asymptomatic hyperuricemia; and new agents such as uricase, which have not been marketed in China.