Gout is also known as “hyperuricemia”, a disorder of purine metabolism, and is a type of arthritis. Gout is a disorder in the metabolism of purine substances in the body, resulting in increased synthesis or decreased excretion of uric acid, causing hyperuricemia, and when the blood uric acid concentration is too high, uric acid is deposited in the form of sodium salts in joints, cartilage and kidneys, causing a foreign body inflammatory reaction, i.e. gout. It is called “gout” because of the severe pain in the joints of the lowest part of the body, which is painful and unbearable, but soon the pain blows over like “wind” in 1-7 days. (95%), and is generally common in women after menopause because estrogen inhibits the formation of uric acid; however, the rate of attacks increases after menopause. Hyperuricemia is not directly related to the occurrence of gout, except that hyperuricemia has a higher likelihood of gout occurring. Some people with hyperuricemia will never trigger gout in their lifetime, while some people will have their first gout within a week or a month of finding hyperuricemia. There is usually a 1-2 year interval after the first gout and also a 10 year interval (5%) during which active treatment is needed to prevent the formation of gout stones. Symptoms Painful inflammation caused by high concentrations of uric acid in the body’s blood, which forms needle-like crystals in soft tissues such as joint membranes or tendons, causing the body’s immune system to overreact (sensitize). The usual sites of attack are the thumb joint, ankle joint, knee joint, etc. In chronic gout, there are cases of attacks in the finger joints and even in the soft tissue of the ear. Acute gout attacks are characterized by redness, swelling, heat, and severe pain, usually at midnight, and can awaken people from sleep. In the early stages of gout, attacks are mostly seen in the lower extremities. Gout can cause kidney damage: Gout can cause kidney damage. According to statistics, 20-25% of gout patients have uric acid nephropathy, and almost 100% of those with nephropathy are confirmed by autopsy. It includes gouty nephropathy, acute obstructive nephropathy and urinary tract stones. 1, gouty nephropathy Persistent hyperuricemia, 20% have clinical manifestations of nephropathy, and after several years or more may successively develop renal tubular and glomerular damage, with a small proportion progressing to uremia. The incidence of urate nephropathy is second only to gouty joint damage and is closely related to the course of the disease and treatment. Studies have shown that urate nephropathy is independent of the severity of gouty arthritis, i.e., patients with mild arthritis can have nephropathy, whereas patients with severe arthritis do not necessarily have renal abnormalities. Mild unilateral or bilateral low back pain is present in the early stages, followed by mild swelling and moderately elevated blood pressure. The urine is acidic, with intermittent or persistent proteinuria, usually not exceeding +++ . Almost always there is a decrease in tubular concentration, nocturia, polyuria, and low relative density of urine. About 5-10 years later, the nephropathy worsens and then develops into uremia, and about 17-25% die of renal failure. The urine of gout patients is acidic, thus increasing the concentration of uric acid in the urine. Smaller stones are excreted with the urine, but they are often not felt, and small brown grains of sand can be seen in the urine sediment; larger stones can obstruct the ureter and cause hematuria and renal colic, and become pyelonephritis due to secondary infection from poor urine flow. Large stones can cause deformation of the renal pelvis and pelvic effusion. When there is sodium urate and calcium salt, the stone shadow can be seen on the X-ray. Acute obstructive nephropathy is seen in the blood uric acid and urine uric acid significantly elevated, that is due to a large number of uric acid crystals extensive obstruction of the renal tubules. Gout is often associated with hypertension, hyperlipidemia, atherosclerosis, coronary artery disease and type 2 diabetes. Cardiovascular factors far outweigh renal insufficiency as a cause of death from gout in the elderly. However, there is no direct causal link between gout and cardiovascular disease, but both are related to obesity and dietary factors. Gout stones, also known as gout nodules, are white crystals that precipitate in a part of the body due to excessive elevation of uric acid in the blood, exceeding its saturation level. As the amount of salt in a glass of salt water exceeds a certain limit, a white deposit will appear at the bottom of the glass. Gout stones can be formed in almost all tissues of a gout patient except the central nervous system. Some gouty stones cannot be seen with the naked eye, but can be seen as white needle-like crystals under a polarized light microscope. These tiny crystals can trigger an attack of gouty arthritis, and can also cause destruction of joint cartilage and bone and fibrosis of the surrounding tissue, resulting in chronic joint swelling, pain, stiffness, deformity, and even fracture. Some gouty stones are deposited on the surface of the body, such as around the ears and joints, and can be seen with our naked eyes. Some gout stones are also deposited in the kidneys, causing kidney stones and inducing renal colic. 5, sex arthritis Mental stress, excessive fatigue, eating a high purine diet, joint injury, surgery, infection, etc. are common triggers. Most patients wake up in the middle of the night with sudden and severe joint pain, accompanied by fever and other systemic symptoms. The early manifestation is monoarthritis, with the first metatarsal and k-toe joints being the most common, followed by the ankle, hand, wrist, knee, elbow and other joints of the foot. If the disease is recurrent, it may develop into polyarthritis, with redness, swelling, heat, pain and limited movement of the affected joints. It is accompanied by fever, with a temperature of 38-39°C. Sometimes there are symptoms such as chills, lethargy, anorexia and headache. Symptoms usually resolve in 1 to 2 weeks. Arthritis subsides, activity is completely restored, and local skin changes from red to brownish red and gradually disappears completely. Flaking and itching may sometimes occur, which are symptoms unique to this disease. The interval can be months or years, and some patients have only one lifetime occurrence, but most patients have a relapse within one year, with one attack or several attacks per year. About 20% to 25% of primary gout patients have kidney stones, of which about 85% are uric acid stones. When the stones are large, there may be renal colic and hematuria. Since uric acid stones are X-rayable, they can only be detected by pyelography. About 20% to 40% of patients may have intermittent small amounts of proteinuria in the early stages. In late stages, interstitial nephritis or kidney stones often lead to renal insufficiency. In addition, patients with gout often have hypertension, obesity, atherosclerosis, and coronary atherosclerotic heart disease.