One morning in mid-July, Mr. Wang, 64, accompanied by his family, limped into the nephrology clinic and said, “Doctor, I have a gout attack” as soon as he entered. After he sat down, we learned that he had been suffering from gout for 2 years, the first attack was 2 years ago, and he had controlled his diet since then, not eating food that could trigger gout, and as a result, he was fine for 2 years. Mr. Wang had already paid attention to diet control, why did he have another attack? The doctor further asked that Mr. Wang likes to eat peanut butter, more than 400 grams of a bottle of peanut butter, nearly a month he has eaten 2 bottles, the result caused the attack. What is nut food? Usually refers to the hard shell of food, in addition to peanuts, there are walnuts, walnuts, cashew nuts, white nuts, chestnuts, almonds, a variety of melon seeds, sesame seeds, etc.. The consumption of these foods can cause an increase in uric acid and induce a gout attack. From Mr. Wang’s example. We can see that although common gout-inducing foods such as mao beans, soybeans and soy products, animal offal, seafood, spinach, mushrooms, and beer are avoided, nutty foods must also be avoided. Although his blood uric acid was within the normal range (420 umol/L), he should still be diagnosed with a gout attack based on his clinical presentation and medical history because some patients do not have high blood uric acid during an attack, but the concentration of uric acid in the tissues is high, so it can still cause joint inflammation. His blood creatinine of 89 umol/L was apparently within the normal range (110 umol/L at the time of the abnormality), but the endogenous creatinine clearance was calculated based on age, weight, and showed that renal function had decreased mildly. He did not have hypertension and diabetes in the past, nor did he have chronic kidney disease; the doctor considered that it was still related to his gout disease. Mr. Wang was not treated when his blood uric acid was usually high, except when he saw a doctor for a gout attack and took medication. When he was asked why he didn’t take medicine, he replied, “I don’t feel uncomfortable, so I don’t care about it”, which is obviously a misconception; there are not many patients like this in our work. Therefore, it is necessary to talk about the danger of “hyperuricemia”. In medical science, people with high blood uric acid but no symptoms are called “hyperuricemia”, and if there is redness and pain in the joints, it is commonly known as “gout”. The typical site is in the cane and toe joints, and the pain is obvious at night; it can also appear in other joints, such as fingers, knees and ankles; these joints have long-term, repeated attacks, which may lead to joint deformities, and some patients may also form gout stones, affecting their lives and work; in addition, chronic interstitial nephritis and uric acid urinary tract stones may appear. Uric acid crystals deposited in the arterial blood vessel wall can cause atherosclerosis, which can cause hypertension or aggravate hypertension; how does high uric acid cause and aggravate hypertension? Studies have shown that high uric acid can stimulate the secretion of renin from the parabolic apparatus of the kidney and decrease the expression of dense plaque neurotype NO (nitric oxide, a vasodilator), both of which can exacerbate the progression of hypertension. The deposition of uric acid crystals in the walls of small arteries directly damages the intima and causes an inflammatory response, while activating the renin-angiotensin system (the body’s blood pressure regulator), resulting in increased blood pressure. High uric acid can also induce cerebral infarction and myocardial infarction; uric acid crystals deposited in the kidneys can cause gouty nephropathy, which can gradually lead to renal insufficiency and even uremia; uric acid crystals blocking the renal tubules can lead to acute renal failure, manifested as oliguria or anuria (24h urine volume less than 400ml or less than 50ml). When you understand the risks associated with hyperuricemia, you will understand the importance of treatment, which is necessary even if you do not feel abnormal, because reducing excessive blood uric acid can prevent these risks from occurring. Is the lower the blood uric acid the better? The answer is no. Medical research has found that uric acid has antioxidant properties, which is a beneficial aspect of the body; so blood uric acid should neither be too high nor too low, otherwise it is equally detrimental to health. Blood uric acid over 417umol/L is considered elevated in men and over 357umol/L in women; the same as men after menopause (phosphotungstic acid oxidation method). Gout is medically divided into primary gout, which is caused by congenital abnormalities or functional defects of purine metabolizing enzymes, and secondary gout, which is caused by decreased uric acid excretion through the kidneys due to various types of renal disease. The treatment of primary gout is slightly different. For primary gout, you can use drugs that inhibit uric acid formation, allopurinol, usually 0.1g 3 times a day, and drugs that promote uric acid excretion, benzbromarone tablets, 50mg once a day; for secondary gout, the effect of drugs that promote uric acid excretion is not good because of renal decompensation, so you should mainly rely on drugs that inhibit uric acid formation, allopurinol, keeping in mind that you can only take 0.1g a day. Above this amount there is a risk of exfoliative dermatitis, which is a serious adverse effect of the drug and can also be life-threatening. Patients with severe renal decompensation should be treated with hemodialysis. For the treatment of gout, you must keep your mouth shut, otherwise the treatment effect will be affected.