Clinical manifestations】 95% of the patients are male, and the age of first attack is usually after 40 years old, but in recent years there is a trend of younger patients; most female patients appear after menopause. According to the natural course of gout, it can be divided into acute, intermittent and chronic phases. 1. Acute phase: There may be no aura before the onset of the disease. Triggering factors include full meals and alcohol, excessive fatigue, stress, localized joint injury, surgery, cold and moisture, etc. Acute monoarthritis, which often strikes at night, is usually the first symptom of gout, manifested as waking up in the early morning with joint pain, progressive aggravation, severe pain like cutting or biting, and pain peaking in 24 to 48 hours. The pain peaks within 24-48 hours. Localized heat, redness, swelling and tenderness in the joints are similar to an acute infection. The first attack is usually monoarthritic, with 60-70% of the first attacks occurring in the first metatarsophalangeal joint, and 90% of patients have recurrent involvement of this part during the course of the disease. The arch, ankle, knee, wrist, and elbow joints are also common sites. It may be accompanied by systemic manifestations, such as fever, headache, nausea, palpitations, chills, discomfort and elevated white blood cells and increased blood sedimentation. 2. Intermittent period: After the acute arthritis attack is relieved, there are usually no obvious sequelae, sometimes only the skin pigmentation of the attack site is deepened, dark red or purplish red, flaking, itching, called asymptomatic intermittent period. Most patients have an interval of 1 to 2 years after the initial attack, but the length of the interval varies greatly, with the interval gradually shortening as the disease progresses. If not prevented, the number of attacks increases each year, the duration of symptoms lengthens, so that it cannot be completely relieved, and the number of joints involved increases, a few patients may have sacroiliac, thoracic lock or cervical spine and other parts of the involvement, and even the involvement of the bursa around the joint, tendons, tendon sheaths and other places can also be seized, the symptoms gradually become atypical. 3.Chronic phase: Repeated deposition of uric acid salt causes chronic foreign body-like reaction in local tissues, surrounded by monocytes, epithelial cells and macrophages, and fibrous tissue proliferation to form nodules, called gout stones. Gout stones are usually found 10 years after the onset of the disease and are a sign that the disease has entered the chronic phase, and can be found in joints, peri-articular areas, subcutaneous tissue and internal organs. They are typically found in the auricle, but also around the joints of the toes, fingers, wrists, ankles, elbows, etc. They are elevated under the skin and appear as yellowish-white sesame- to egg-sized bullae with a thin surface, and when they break down, they discharge a white powder or paste that does not heal over time, but rarely become infected. When gouty stone occurs in the joint, it can cause joint cartilage and bone erosion and destruction, hyperplasia, periarticular tissue fibrosis, persistent joint swelling and pain, ankylosis, deformity, and even fracture, called gouty stone chronic arthritis. 4. renal lesions: renal pathology is almost always damaged, and about 1/3 of patients develop renal symptoms during the course of gout. (1) Uric acid nephropathy: Uric acid crystals are deposited in the renal tissue, especially in the renal medulla and conus, which can lead to chronic interstitial nephritis, deforming, atrophying, fibrosis and sclerosis of the renal tubules, and then involving the glomerular vascular bed. It manifests as back pain, edema, hypertension, decreased tubular concentration function, increased nocturia, low specific gravity urine, hematuria, proteinuria, and advanced renal insufficiency. (2) Uric acid urinary stones: uric acid concentration in urine increases and deposits to form urinary stones, which have a total incidence of more than 20% in gout patients and may appear before the onset of gouty arthritis. Smaller stones are excreted in the urine in the form of gravel and can be asymptomatic. Larger ones obstruct the urinary tract and cause renal colic, hematuria, pyelonephritis, and hydronephrosis. Due to the low pH of urine in gout patients, uric acid is mostly converted into uric acid, which is less soluble than uric acid, so it is easy to form pure uric acid stones, which often do not show up on X-rays. (3) Acute uric acid nephropathy: Mostly seen in secondary hyperuricemia, mainly seen after tumor radiotherapy and chemotherapy, blood and uric acid suddenly and significantly increased, a large number of uric acid crystals deposited in renal tubules, collecting ducts, renal pelvis, ureter, causing extensive and serious urinary tract obstruction, manifested as oliguria, anuria, acute renal failure, a large number of uric acid crystals and red blood cells visible in urine.