Gouty nephropathy

　　The causes of gouty nephropathy are increased uric acid concentration in blood and (or) urine. The factors that increase uric acid concentration include:

　　1. Genetic factors

　　Enzyme gene mutations can lead to increased uric acid concentration, such as the deficiency of hypoxanthine-guanine phosphoribosyltransferase.

　　2. Acquired factors

　　Marrow hyperplasia, high purine intake, excessive obesity, hypertriglyceridemia, excessive dietary fructose content, and high alcohol content in beverages can all lead to increased uric acid concentration. Uric acid is the final product of purine metabolism, and it is a trioxide purine, mainly derived from the metabolism and decomposition of nucleic acids and other purine compounds in cells. Uric acid is produced from purines in food through the action of enzymes. The main reasons for excessive endogenous uric acid production include the decreased activity of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and the increased activity of phosphoribosylpyrophosphate amidotransferase (PRPP) and hypoxanthine, xanthine oxidase (XO).

　　The most serious complication of gouty nephropathy is renal failure. The deterioration of chronic gouty nephropathy caused by hyperuricemia is an important cause of renal failure, especially in patients with recurrent gout for more than ten years, combined with hyperlipidemia, hypertension, high cholesterol, hyperglycemia, obesity, and gouty stones, which are common in middle-aged and elderly people, and men are more than women. The three lesions leading to renal failure due to renal damage include gouty nephropathy, acute obstructive nephropathy, and urinary tract stones.

　　Renal failure is a pathological condition in which the function of the kidneys is partially or completely lost. It is divided into acute and chronic types according to the urgency of onset. Acute renal failure is caused by various diseases that result in the loss of excretory function of both kidneys in a short period of time, abbreviated as acute renal failure. Chronic renal failure is a comprehensive syndrome composed of a group of clinical symptoms that occur when chronic kidney disease develops to a late stage due to various causes.

　　Gouty nephropathy is mainly caused by damage from gout, and its clinical manifestations include:

　　1. Early stage

　　Early patients may have significant hypertension and azotemia, and 25% of patients may have urinary tract infections during the course of the disease. Generally, gouty nephropathy often develops unnoticed and progresses slowly, often taking 10 to 20 years before renal failure occurs. There are also about 20% of patients with concurrent uric acid stones, which may cause renal colic, hematuria, or urination of uric acid stones.

　　2. Middle stage

　　Patients entering this stage have obvious changes in routine urine tests, with proteinuria becoming persistent, and red blood cells or casts may be found. Patients may have mild edema and hypoalbuminemia. Some patients may have symptoms such as high blood pressure, backache, fatigue, dizziness, and headache. If related renal function tests (such as creatinine clearance rate, phenol red excretion test, glomerular filtration rate measurement, etc.) are performed, mild to moderate renal function impairment may be found, but blood urea nitrogen and creatinine levels will not increase significantly.

　　3. Late stage

　　In the late stage, symptoms such as edema, hypertension, hypoalbuminemia, and anemia are more obvious, and anemia may occur. The most prominent manifestation is the aggravation of renal insufficiency, with the gradual decrease in urine output, progressive increase in blood urea nitrogen and creatinine, and the occurrence of significant azotemia. Finally, it develops into uremia and renal failure, which can only be maintained by artificial kidneys.

　　Patients with long-standing gout may have gouty nephropathy in about 1/3, so for gout patients, especially those with long-standing disease, there must be a consciousness of preventing gouty nephropathy, combining syndrome differentiation with disease differentiation, reducing the recurrence of gout, and preventing the occurrence of gouty nephropathy.

　　For patients with asymptomatic hyperuricemia, the prevention of gout attacks is mainly non-drug treatment, including dietary control and abstinence from alcohol, and avoiding drugs that increase blood uric acid levels such as diuretics, low-dose aspirin, compound antihypertensive tablets, pyrazinamide, nifedipine, and propranolol, etc. If blood uric acid is still above 9mg/dl after dietary control, uric acid-lowering drugs can be used. For patients who have had acute gouty arthritis and are in the intercritical period, preventive measures should be taken to prevent the recurrence of gout, the key being to control blood uric acid levels through diet and drug treatment to meet the standard, and in addition, attention should be paid to avoiding strenuous exercise or injury, controlling body weight, drinking plenty of water, and long-term alkalinization of urine, etc.

　　Gouty nephropathy is caused by gout, and patients with long-standing gout may have renal damage in about 1/3. In treating patients with gouty nephropathy, in addition to active treatment, regular checks should be performed, mainly including the following:

　　1. Blood examination

　　The blood routine examination of gouty nephropathy patients shows an increase in white blood cell count, an increase in erythrocyte sedimentation rate, an increase in blood uric acid, male above 0.38 mmol/L, and female above 0.3 mmol/L before menopause, and the same as males after menopause.

　　2. Urine examination

　　Patients may have intermittent proteinuria, low urine specific gravity, and high uric acid content in urine (normal: 0.38-5.59 mmol/24 hours urine).

　　3. Renal pelvis and ureteral venography and B-ultrasound

　　Renal pelvis and ureteral venography and B-ultrasound can detect renal calculus shadows.

　　4. Synovial fluid examination

　　The examination of synovial fluid under polarized light microscopy can reveal needle-shaped uric acid crystals with birefringence in white blood cells.

　　The diet of gouty nephropathy patients is the same as that of gout patients, both of which require low-purine and salt restriction.

　　1. Low-purine diet

　　Patients should adopt a low-purine diet in their daily life. It is advisable to choose foods with low purines, such as flour, onions, fruits, milk, eggs, etc.; avoid foods with high purines, such as animal internal organs, brain, and various broths, broths, sardines, mackerel, and anchovies; coarse grains, spinach, cauliflower, mushrooms, broad beans, and animal and poultry meats contain purines, and should be chosen carefully.

　　2. Limit salt

　　Patients should limit the intake of sodium salt, and 2-5 grams per day is appropriate.

　　3. Drink more water

　　Patients should drink 2500-3000 milliliters of water each day, eat more fruits and foods with high water content, increase urine output to help the kidneys excrete uric acid, and reduce the damage of uric acid to the kidneys.

　　4. Eat more alkaline foods

　　Patients should eat more vegetables and fruits, which are alkaline foods. Alkaline environment can increase the solubility of uric acid, and these substances are rich in vitamin C, which can promote the dissolution of uric acid in tissues and is conducive to the excretion of uric acid. Generally, 1 kilogram of vegetables (vegetables containing purines should be avoided) and 4-5 times of fruit should be eaten daily.

　　5. Avoid刺激性 food

　　Patients should avoid spicy and刺激性 food, quit smoking and drinking. It was previously believed that gout patients should avoid tea, but now it is considered that these substances do not produce uric acid in the body metabolism, and there is no deposition of痛风 stones, so they can be moderately selected.

　　For the treatment of gout and how to prevent and treat gouty nephropathy in traditional Chinese medicine, dialectical treatment should be carried out. Detailed description as follows:

　　1. Lower Jiao Damp-Heat Syndrome

　　Treatment Method: Clear heat, dry dampness, and promote diuresis.

　　Prescription: Four Miraculous Powder with Modification.

　　Astragalus 12g, Phellodendron 10g, Coix Seed 12g, Achyranthes 10g, Herba Angelicae Sinensis 10g, Stephania Root 10g, Chinese Skullcap 10g, Smilax Glabra 30g, Bombyx Seed 10g (decocted in a bag), Prunella Leaf 60g. The formula uses Atractylodes to dry dampness, Phellodendron to clear heat as the main medicine, Coix Seed, Smilax Glabra, Bombyx Seed, and Stephania Root to dilute and promote diuresis, Achyranthes, Herba Angelicae Sinensis, Chinese Skullcap, and Prunella Leaf to unblock collaterals and relieve pain. Thus, damp-heat is differentiated, Qi and blood circulation is improved, and swelling and pain will naturally subside. For those with excessive heat in the lower jiao, add Phellodendron, soaked in wine, dried and ground into fine powder, take 3g each time, twice a day. This formula is for internal use. For severe pain, add 3-5g of prepared Myrrha; for severe swelling, add Pericarpium Arecae, Areca Nut, Alisma, and Rhizoma Amorphophallus; for increased phlegm, add Naphthalene, Pinellia, and White Mustard Seed.

　　中成药：二妙丸。

　　2、瘀血阻络证

　　治法：活血化瘀，宣痹止痛。

　　方药：桃红四物汤加减。

　　生地12g，当归10g，赤芍10g，川芎10g，桃仁10g，红花10g，威灵仙10g，秦艽10g，鸡血藤10g，防风10g，徐长卿12g，桑枝10g。方用四物汤养血活血，桃仁、红花活血化瘀，威灵仙、桑枝、防风、徐长卿等宣通经络，合奏活血、宣痹之功。无热象者可加桑枝；痛甚加姜黄、海桐皮；挟痰加制南星、白芥子；瘀滞日久，其痛日轻夜重，局部黯黑者，可配服活络效灵丹（当归、丹参、乳香、没药）以增强活血化瘀的作用。

　　中成药：瘀血痹冲剂。

　　3、痰热挟风证

　　治法：清热燥湿，化痰祛风。

　　方药：上中下痛风方。

　　黄柏10g，苍术10g，防风10g，威灵仙10g，白芷10g，桃仁10g，川芎10g，桂枝10g，羌活10g，龙胆草6g，炮南星10g，红花6g。方用黄柏、龙胆草清热，苍术、南星燥湿，羌活、防风、白芷祛风，桃仁、川芎、红花活血，桂枝一味有温经通络之长，丹溪谓能“横行手臂，领苍术、南星等药至痛处。”痰多加半夏、白术、茯苓、陈皮。

　　中成药：风湿稀桐丸。

　　4、气血两虚证

　　治法：行气养血为主。

　　方药：对愈汤加减。

　　黄芪30g，党参15g，熟地黄12g，当归10g，山药15g，白术10g，川芎10g，白芍12g。方用参、芪补气，熟地、当归、川芎、白芍养血活血，山药、白术健脾。脾气壮血活，经脉通畅，酸软疼痛自已。夹风湿者，可酌加羌活、防风、稀莶草、桑枝之类，但不可纯作风治，否则反燥其白，终不能愈；挟湿热者，加酒炒黄柏；挟痰浊者加制南星、姜汁；病久肾阴不足可加龟板、肉苁蓉、怀牛膝。

　　中成药：八珍丸、十全大补丸。