Every disease has a process that gradually worsens as it progresses. This section introduces you to the stages of the gout disease process. I. Asymptomatic hyperuricemia stage Patients with increased blood uric acid concentration, but without joint pain caused by arthritis, are called asymptomatic hyperuricemia. The period from the increase of blood uric acid to the appearance of symptoms can last for years to decades, in general. The higher the uric acid level, the higher the risk of developing gout, which is only called gout when arthritis occurs. Some people with hyperuricemia do not develop symptoms for the rest of their lives. Second, acute gouty arthritis (gout attack phase) If hyperuricemia persists and is not taken seriously, it enters the gout attack phase. Triggers include overeating, overexertion and stress, often with a sudden onset and redness, swelling, heat and painful restricted movement of the affected joints within a few hours. The initial attack is usually uni-articular, with subsequent involvement of multiple joints. Unilateral bunions and the first metatarsophalangeal joint (the joint between the bunion and the metacarpal) are the most common, followed by the ankle, knee, wrist, finger, and elbow. It may be accompanied by systemic symptoms such as fever, headache and elevated white blood cells. Gout attack interval The initial symptoms of gout attack last for several days to weeks and then resolve naturally, leaving no sequelae and entering the asymptomatic phase called interval. If the intermittent period does not reduce the blood uric acid concentration to the ideal value (<300μmol/L or <360μmol/L), the number of gout attacks will become more frequent, and the pain will last longer and become more severe as time goes by. More than half of the patients will have a relapse within the first year, and only a very small number of patients will have only one attack in their lifetime. Therefore, one should not be lucky and paralyzed at this stage, and should actively lower uric acid to stop gout attacks. Fourth, gout stone and chronic gouty arthritis stage Patients with persistently elevated hyperuricemia can avoid entering this stage if they are prevented from doing so by medication and diet early on Patients in this stage are mostly seen in patients who have not been treated or have poor treatment results. Long-term hyperuricemia results in the formation of uric acid crystals, which are deposited in cartilage, synovial membranes, tendons and soft tissues, forming yellowish-white gout nodules as large as sesame seeds to eggs, called gout stones. Gout stones are mostly found in the joints of the ears and extremities. As the disease progresses, excessive gout stone formation and recurrent gout attacks can lead to joint stiffness, restricted movement and deformity. In the later stages of the disease, the intervals are shortened and the pain becomes increasingly severe, even after the attack cannot be completely relieved. V. Nephropathy 1/3 of patients with gout may develop nephropathy due to recurrent attacks involving the kidneys. Types of nephropathy include: 1. Uric acid nephropathy is caused by the deposition of uric acid in the interstitial tissues of the kidney. In the early stage, it may manifest only as intermittent proteinuria and microscopic hematuria. As the lesion progresses, impaired renal concentration function, chronic renal insufficiency and renal failure (uremia) may develop. Some patients have uric acid nephropathy as the first clinical manifestation. 2, renal uric acid stones primary gout patients 20% to 25% of patients appear renal uric acid stones. Small sediment-like stones can be excreted in the urine without symptoms, while larger stones can cause renal colic, hematuria and urinary tract infection. Renal uric acid stones may be the first clinical manifestation in some patients. The incidence of renal uric acid stones is higher in patients with secondary gout who have tumor dissemination or received radiotherapy. 3. Acute renal failure A large number of uric acid crystals block the urinary tract (renal tubules, renal pelvis or ureter), and the patient suddenly develops oliguria or even anuria, and acute renal failure occurs.