Chronic renal failure, also known as chronic renal insufficiency, is a clinical syndrome caused by chronic progressive renal parenchymal damage from various causes, resulting in significant atrophy of the kidneys and inability to maintain their basic functions, with clinical manifestations of metabolite retention, imbalance of water, electrolytes and acid-base balance, and systemic involvement, also known as uremia. Chronic renal failure is referred to as chronic renal failure, due to the destruction of renal units and the reduction of renal excretory regulation and endocrine metabolic function, resulting in a series of symptoms, signs and complications of water and electrolyte, acid-base balance disorders. The cause of pediatric chronic renal failure is closely related to the age of the child at the time of the first detection of renal failure. Chronic renal failure under 5 years of age is often the result of anatomical abnormalities, such as renal hypoplasia, abnormal renal development, urinary tract obstruction, and other congenital malformations; chronic renal failure after 5 years of age is dominated by congenital glomerular diseases such as glomerulonephritis, hemolytic uremic syndrome, or genetic lesions such as Alport syndrome and renal cystic lesions. In chronic kidney diseases, as the disease deteriorates, the progressive destruction of renal units, so that the remaining functional renal units are insufficient to adequately excrete metabolic waste and maintain a constant internal environment, resulting in urinary dysfunction and internal environmental disorders, including retention of metabolic waste and toxic substances, water, electrolyte and acid-base balance disorders, and a series of clinical symptoms of the pathological process, known as CRF (chronic renal failure). Chronic renal failure Severe chronic renal failure, when called uremia, is not an independent disease, but a combination of symptoms that occur when various etiologies cause kidney damage and progressive deterioration, when it develops to the end stage and renal function is close to about 10% of normal. As renal function damage is a longer development process, different stages, with their different degrees and characteristics, should generally be divided into several stages according to the level of renal function. Renal function compensatory stage When the damage of renal function units does not reach 1/2 of the total number, it does not produce elevated blood urea nitrogen and creatinine, metabolic balance in the body, and no symptoms appear (with blood (Scr) creatinine at 133-177 μmol/L (2 mg/dl)). Stage of renal insufficiency The level of renal function drops below 50%, the level of blood (Scr) creatinine rises above 177μmol/L (2mg/dl), the level of blood urea nitrogen (BuN) rises >7.0mmol/L (20mg/dl), and the patient has symptoms such as weakness, loss of appetite, nocturnal urination, and mild anemia. Renal failure stage When endogenous creatinine clearance (Ccr) drops below 25ml/min, BuN level is higher than 17.9 – 21.4mmol/L (50~60mg/dl), Scr rises above 442μmol/L (5mg/dl), the patient develops anemia, rising blood phosphorus level, falling blood calcium, metabolic acidosis, water and electrolyte disorders, etc. End stage of uremia Ccr is below 10ml/min, Scr rises above 707μmol/L, acidosis is obvious, and symptoms of various systems appear, even coma. Disease symptoms pay attention to the presence of nausea, vomiting, diarrhea, unbearable burning pain in the lower limbs subject to frequent movement, skin itching, bone pain, convulsions and signs of bleeding. Physical examination: pay attention to the respiratory rate and depth, the presence of ammonia smell, the state of mind, the degree of anemia, the presence of muscle twitching, water loss, edema, oral mucosal ulcers, pericardial friction sounds, blood pressure and the presence of signs of heart failure. Disease etiology Note the presence of acute and chronic nephritis, acute and chronic pyelonephritis, small renal arteriosclerosis, renal tuberculosis, urinary tract obstruction, systemic lupus erythematosus, diabetes mellitus, gout, multiple myeloma and polycystic kidney, as well as a history of long-term use of antipyretic analgesics and exposure to heavy metals. Points to note: 1, should strive to clarify the etiology of chronic renal failure, at least should clarify whether the kidney damage is mainly glomerular damage, or interstitial tubular lesions, or renal vascular lesions prominent, so that according to the clinical characteristics, treatment has a focus. 2. The reversible factors that contribute to the progressive development of renal function in chronic renal failure should be identified, such as infection, metabolic acidosis, dehydration, heart failure, rapid and low blood pressure reduction, etc. 3. Attention should be paid to finding certain factors that exacerbate the progressive decline of renal function in chronic renal failure, such as hypertension, hyperlipidemia, hypercoagulability, high protein dietary intake, large amount of proteinuria, etc. Disease pathology mechanism of progressive glomerular damage: According to clinical observation, patients with uremia have a regular progression of the disease process, which is a progressive deterioration. If according to the above staging, when the patient enters the stage of renal insufficiency and the blood creatinine reaches the level of 442umol/L (5mg/dl), the average time to develop into end-stage uremia is 10.8 months. The main mechanisms are the following theories: 1. Glomerular hyperfiltration theory It is believed that the important cause of the progression of uremia is due to the hyperfiltration of glomeruli in the residual kidney units, which eventually leads to glomerulosclerosis. It is known that when renal parenchyma is reduced, such as after partial nephrectomy, the individual glomerular filtration rate of the residual renal unit increases and the resistance of the small glomerular input and output arteries decreases, thus increasing the individual glomerular blood flow rate. At the same time, the resistance of the small input arteries is reduced to a greater extent than that of the small output arteries, contributing to an increase in the hydrodynamic pressure gradient across the glomerulus capillaries. These constitute an increase in the glomerular filtration rate (GFR) of the residual kidney unit, and the degree of increase correlates with the degree of parenchymal reduction, with an average increase of 40 to 50% if one side of the nephrectomy is removed, while the increase in GFR of the residual kidney is twice as large as normal after 80% of the parenchyma is removed. According to the experiment, SNGFR=K1*PnFK1= ultrafiltration coefficient and PnF= mean net ultrafiltration pressure. From the above equation, it can be seen that the magnitude of these two values, determines the size of SNGFR. k1 even when there is a large decrease in renal units, the K1 of the glomerulus of the residual renal units does not change much, and PnF plays a decisive role in increasing SNGFR. the size of PnF in turn depends on three factors: ① capillary hydrostatic pressure difference (ΔP); ② plasma protein concentration (CA); ③ glomerular plasma flow (QA). When a kidney unit is lost and the residual kidney unit “compensates” or “adapts”, both △P and QA increase with each other, thus increasing SNFFR. This hyperfiltration, although a compensatory effect, in turn, causes glomerular damage in the residual renal unit. As seen in 85% of nephrectomized animals, at 3 months residual glomerular hypertrophy, epithelial cell exfoliation, progressive enlargement of the thylakoid zone and loss of capillary lumen elasticity finally lead to focal, segmental glomerulosclerosis. On the other hand, increased capillary pressure and blood flow encourage macrophages to move outside the capillaries and into the thylakoid zone, all of which contribute to glomerulosclerosis. These changes cause further reduction of renal units, resulting in increased filtration rate of residual glomeruli, new lesions and new sclerosis, forming a vicious circle and worsening of the disease. 2.The doctrine of imbalance of correction In uremia, certain humoral factors that cause toxic effects gradually increase in body concentration, not entirely due to the reduction of renal clearance, but a balanced adaptation of the body; but in the process of adaptation, there is a new imbalance, and so on and so forth, causing progressive damage to the body. For example, in the case of blood thyroid hormone (PTH), GFR decreases in uremia, urinary phosphorus excretion decreases, and hyperphosphatemia occurs, which stimulates the parathyroid glands to secrete PTH, which acts on the renal tubules to increase urinary phosphorus excretion, so that blood phosphorus decreases and returns to normal levels. However, due to more loss of renal function, PTH continues to rise at the extracellular fluid level, which still makes it difficult to correct hyperphosphatemia, while causing an increase in serum calcium product and an increase in intracellular calcium, resulting in extensive deposition of calcium and phosphorus in multiple systems throughout the body, including the kidneys themselves. When GFR decreases further, hyperphosphatemia occurs again. This cycle results in increasing plasma PTH levels and further destruction of the renal unit. In uremia, serum and urinary natriuretic hormone levels are elevated, suggesting that reduced renal clearance is not the cause of its elevation and that probably increased in vivo production is the main factor. In uremia, GFR decreases, sodium excretion tends to decrease, and the residual renal units become compensated for hypertrophy, and osmotic diuresis caused by urea accumulation is no longer able to regulate sodium balance. PTH natriuretic hormone itself is not a “toxic” substance, but under the above circumstances, its level in the body increases continuously, forming a new “toxin”. “toxin”. The doctrine of hyperfiltration, which explains the main cause of progressive glomerular damage in uremia, provides the theoretical basis for the prevention and treatment of uremia. The doctrine of correction of imbalance, focusing on the formation of uremia, the body imbalance, the production of certain excessive substances, can form uremic symptoms, treatment of these imbalances, can reduce the occurrence of symptoms, such as partial removal of parathyroid glands, or trying to control secondary hyperparathyroidism, is of great significance in the alleviation of uremic symptoms. 3, “toxin” theory Currently it is known that there are more than 200 substances in the body of uremic patients with elevated concentrations, which may have toxic effects, about 20 kinds. These substances have the following characteristics: ① the substance can be published chemical identification and quantitative determination. ②Higher than normal concentration levels in the body. ③High concentrations are associated with specific uremic symptoms. ④Experimentally confirmed similar toxic effects when the concentration of the substance is similar to the concentration in the body fluid of uremic patients. The mechanism of progressive deterioration of chronic renal failure its mechanism is not yet fully understood. The deterioration of renal function is undoubtedly related to the activity of the underlying disease. However, although the underlying disease has ceased to be active, such as when the GFR has fallen to about 25% of normal, renal function continues to decompensate incessantly until uremia develops, and its decompensation is through a common pathway. Most scholars now believe that when a certain number of kidney units are destroyed, the metabolic waste excretion load of the remaining “surviving” kidney units increases to maintain the normal needs of the body. As a result, glomerular capillary hyperperfusion, hyperpressure and hyperfiltration (glomerular “triple high”) occur compensatorily. The “three highs” in the glomerulus can cause: (1) fusion of glomerular epithelial cells, significant proliferation of thylakoid cells and stroma, glomerular hypertrophy and subsequent sclerosis; (2) damage to glomerular endothelial cells, which induces platelet aggregation and leads to microthrombosis, damaging the glomerulus and promoting sclerosis; (3) increased glomerular permeability, which increases proteinuria and damages the tubular interstitium. (3) Increased glomerular permeability increases proteinuria and damages the tubular interstitium. The above processes continue, forming a vicious circle, making kidney function deteriorate further. This is the common pathway for all chronic kidney diseases to develop into uremia. Angiotensin II (AII) plays an important role in the progressive deterioration of renal failure. In the glomerular “three highs”, the activity of renin and angiotensin axis increases, and AⅡ is a powerful vasoconstrictor. Whether it is the systemic circulation of AⅡ that causes hypertension, or the local AⅡ increase in the kidney, it can lead to the increase of glomerular capillary pressure, causing glomerular hypertrophy and then glomerulosclerosis. In addition, AⅡ also causes the following effects independent of blood pressure: ① Involved in extracellular matrix (ECM) synthesis, and excessive accumulation of ECM will cause glomerulosclerosis; ② AⅡ will increase transforming growth factor β1 (TGF-β1), platelet-derived growth factor (PDCF), interleukin-6 (IL-6), platelet-activating factor (PAF), thromboxane A2 ( TXA2) and other growth factors, inflammatory factors and fibrotic factors are expressed, while TGF-β1 is a determinant mediator of renal ECM synthesis and fibrosis, which contributes to the development of glomerulosclerosis. AII increases glomerular capillary blood pressure, which causes increased glomerular permeability and excessive protein filtration from the glomerulus, which is absorbed by proximal tubular cells through cytosolic drinking, and can cause tubular damage, interstitial inflammation and fibrosis, resulting in loss of renal unit function. Studies have shown that the uptake of albumin by proximal tubular cells in culture increases the expression of growth factors, inflammatory factors and fibrotic factors. Proteinuria is now considered to be an important factor in the progressive deterioration of renal failure. In recent years, it is believed that the rate of deterioration of renal failure is genetically related, such as the angiotensin-converting enzyme gene has an important relationship with the rate of renal decompensation. The disease is characterized by nausea and vomiting, dullness, foul-smelling urine in the mouth, excessive or scanty urination at night, edema, lumbago, weakness, fatigue, headache, irritability, epistaxis, lack of color, and nail fault in the skin, etc. The disease can be classified as “Guange”, “Drowning Poison” and “Void Labor” in Chinese medicine. The main clinical manifestations of the disease are “Guan Ge”, “Drowning Poison”, “Void Labor” and so on. The key to the pathogenesis is the lack of power of qi-transformation in the Sanjiao and the stagnation of dampness and toxicity; the disease is located in the kidneys and affects the five viscera and six internal organs. The disease is mostly critical, with a poor prognosis, manifesting as a disorder of yin and yang, mixed evidence of deficiency and reality. In the early stage of clinical manifestations, the disease is often manifested only as symptoms of the underlying disease. 1, the residual kidney units can not adjust to the requirements of the body, the symptoms of renal failure 2, renal failure is very complex, can involve all organs of the body, constituting uremic manifestations 3, dialysis can improve most of the symptoms of uremia, but some symptoms can continue or even aggravate the symptoms of each system: 1, gastrointestinal tract: is the earliest, the most common symptoms Performance: a. Anorexia (loss of appetite earliest) b. Nausea, vomiting, abdominal distension c. Tongue and mouth ulcers d. Ammonia odor in the mouth e. Upper gastrointestinal bleeding, etc. 2. Hematologic system: a. Anemia: It is a necessary symptom for uremic patients. The degree of anemia is parallel to the degree of uremia (renal function), erythropoietin (EPO) is reduced as the main cause b. Bleeding tendency: can be manifested as skin, mucous membrane bleeding, etc., with increased platelet destruction, prolonged bleeding time, etc., may be caused by toxins, dialysis can be quickly corrected c. Leukocyte abnormalities: reduced, chemotaxis, phagocytosis and bactericidal ability, prone to infection, dialysis can be improved 3. Cardiovascular system: the most common cause of death in renal failure a. Hypertension: most patients have varying degrees of hypertension volume dependent + renin dependent Can cause atherosclerosis, left ventricular hypertrophy, heart failure b. Heart failure: often manifestations of cardiomyopathy, water and sodium retention; hypertension; uremic cardiomyopathy, etc. c. Pericarditis: uremic or due to inadequate dialysis, mostly hematogenous, usually late manifestations d. Atherosclerosis: rapid progression, more so in hemodialysis, can occur in coronary arteries, cerebral arteries, systemic peripheral arteries mainly due to hyperlipidemia and hypertension 4. Neurological and muscular system manifestations: a. Early stage: fatigue, insomnia, inattention, etc. b. Late stage: peripheral neuropathy, sensory nerves are more significant than motor nerves c. Dialysis imbalance syndrome: too rapid reduction of urea nitrogen, imbalance of intra- and extracellular osmotic pressure caused by increased intracranial pressure and cerebral edema, manifesting nausea, vomiting, headache, and convulsions in severe cases. 5. renal bone disease: is a general term for skeletal changes in uremia a. can cause spontaneous fractures b. rare with symptoms, such as bone pain, walking difficulty, etc. 6. respiratory manifestations: a. deep and long breathing in acidosis b. uremic bronchitis, pneumonia (butterfly wing), pleurisy, etc. 7. skin symptoms: pruritus, urea cream deposits, uremic facies, which cannot be improved by dialysis 8. endocrine disorders: a. Hormones produced by the kidneys fall b. Hormones degraded in the kidneys can rise 9. easily complicated by serious infections: fever is not as obvious as in normal people when infected 10. metabolic disorders and others: a. hypothermia: body temperature is lower than normal by about 1oC (should be considered when estimating fever), basal metabolic rate often decreases b. abnormal glucose metabolism: ordinary patients: reduced glucose tolerance; diabetic patients: insulin dosage should be reduced (degradation c. Abnormal lipid metabolism: normal TC d. Hyperuricemia: GFR <20, impaired clearance of uric acid, rare occurrence of gouty arthritis Diagnostic tests 1, test routine blood, platelets, bleeding and clotting time, prothrombin time, blood urea nitrogen, creatinine, uric acid, carbon dioxide binding capacity, blood gas analysis, blood glucose (fasting, 2h after meal), blood lipids, serum potassium, sodium, chloride, calcium, phosphorus Magnesium, alkaline phosphatase, plasma protein, protein electrophoresis, urine routine, urine specific gravity, 24h urine protein quantification, 24h urine potassium, sodium, chloride, calcium, phosphorus, urea nitrogen, creatinine, uric acid quantification, endogenous creatinine clearance, morning urine osmolality measurement. Other tests: fundus, electrocardiogram and ultrasound of both kidneys, renal nuclear test, chest X-ray, abdominal plain film and bone film if necessary. 4.Stage of renal insufficiency ①Compensation stage: renal unit damage does not exceed 50%; GFR50～80ml/min, Scrl33～177μmol/L, no clinical symptoms; ②Decompensation stage: GFR50～20ml/min, Scr 186～442μmol/L, clinical weakness, mild anemia, loss of appetite and other systemic symptoms; ③Renal function (3) renal failure stage: GFRl0-20ml/min, Scr451-707μmol/L, patients have severe anemia, metabolic acidosis and disorders of water-electrolyte metabolism; (4) uremic phase: GFR<10ml/min, Scr>707μmol/L, clinically aggravated metabolic acidosis and prominent symptoms of various systems. Treatment plan Conventional treatment 1. Care according to the care routine of kidney disease. 2. Pay attention to the mental and respiratory conditions, any nasal bleeding or skin and mucous membrane bleeding. Those with mental abnormalities or convulsions or convulsions must prevent self-injury, and those in coma should be cared for according to the coma care routine. 3. Diet treatment. ①Give low protein, high calorie, vitamin-rich diet. Use eggs, milk and other high-quality protein, daily intake: 25-35g/d of protein for endogenous creatinine clearance >lOml/min, blood urea nitrogen 10.7-25.1mmol/L, blood creatinine 265.2-618.8μmol/L; endogenous creatinine clearance 5-lOml/min, blood urea nitrogen 25.1-36mmol/L, blood creatinine 618.8～884μmol/L, give 20～25g/d of protein, and keep the daily caloric energy above 146kJ(35kcal)/kg preferably. (②In the low protein diet at the same time oral essential amino acids, dose 0.1-0.2g/(ks?d), divided into 3-5 times to take water, for serious gastrointestinal symptoms can be short-term intravenous drip 250ml/d. (③Low protein diet plus α-keto acid treatment, to open the same for example: 3/d, 1.6-3.2g/time, pay attention to review the blood calcium concentration, contraindicated in hypercalcemia. The staple food should be wheat starch with de-vegetated protein. In the absence of severe hypertension and obvious edema, urine volume >1000ml/d, salt 2~4g/d, potassium intake is not strictly limited. 4.Chinese herbal medicine treatment. For those who have Yang deficiency, it is appropriate to strengthen the spleen and kidneys, and tonify both qi and blood, and add Xianmao, Epimedium, Cuscuta and other Yang-aiding drugs; for those who have spleen and kidney failure and dampness, it is appropriate to lightly percolate and benefit dampness, and flatly tonify the spleen and kidneys. The Chinese medicine rhubarb is effective in delaying the progression of renal function in chronic renal failure. 5. Pay attention to water and electrolyte balance. If there is water loss or hyponatremia, it should be corrected in time. For high blood phosphorus and low blood calcium, give 1g of calcium carbonate, 3/d or oral 1,25 dihydroxyvitamin D3, 0.25-0.5μg/d, and adjust the dose according to the blood calcium concentration. 6. In mild acidosis, compound citrate solution (1000ml containing 140g of citrate and 98g of sodium citrate) can be taken, 40-90ml/d, in 3 doses. If the carbon dioxide binding capacity <13.5mmol/l (30 volume %) and there are symptoms of acidosis, use 5% sodium bicarbonate 200ml IV, or 11.2% sodium lactate lOOml diluted to 600ml IV. If edema is obvious and blood pressure is too high, 3.64% aminobutriol (THAM) 200ml IV can be used. 7. Those with infectious factors should be actively controlled by antibiotics. 8, can try adsorbent, such as oxidized starch 30-50g / d, divided internal; medicinal charcoal 40g / d, divided internal, has the effect of reducing blood urea nitrogen. 9, urine less, edema obvious people available furosemide (tachyphylaxis) 40 ~ 100mg sedation, 1/6 ~ 8h, or butylamine lmg, 1/6 ~ 8h. But prohibit potassium-protective diuretics, so as not to aggravate hyperkalemia. 10, obvious hypertension with antihypertensive drugs, to choose A-CEI mainly, such as mercaptomethoproline (25-100mg, 3/d), enalapril (5-10mg, 1/d), benazepril (5-20mg, 1/d), the principle of medication as acute nephritis, antihypertensive should not be too fast, excessive, to maintain diastolic blood pressure at 13.3kPa (100mmHg) is appropriate, should not reduce The urine volume should not be reduced, and the occurrence of hyperkalemia should be observed. In cases of heart failure, digitalis preparations can be used, but the dose should be reduced by 1/2 to 1/3 compared to the usual amount. severe anemia can be treated with erythropoietin, subcutaneous injection 2-3 times/week, 1500-3000 U/time. In case of bleeding, blood transfusion is appropriate. In case of nausea and vomiting, metoclopramide (gastrofluan), domperidone (morpholine) or chlorpromazine (dormantine) can be used. 11, dialysis therapy: those who have the conditions should be implemented in a timely manner. 12. Allogeneic kidney transplantation: those with indications and conditions to receive transplantation, and with appropriate immune selection of the recipient and donor can be performed. Micro-Chinese medicine infiltration therapy In the treatment of chronic renal failure, "micro-Chinese medicine infiltration therapy" is used for treatment. Micro-Chinese medicine infiltration therapy is actually a systematic treatment to stop the process of kidney fibrosis by micro-Chinese medicine infiltration therapy, which guides the formulation and implementation of medication and treatment measures for kidney failure patients based on the latest kidney disease diagnosis theory. Its core technology is to micronize the Chinese medicine for kidney disease and then evenly distribute it in the two kidney areas and infiltrate it with the micronization therapy instrument. The treatment of kidney failure micro-chemical Chinese medicine infiltration therapy and combined with western medicine symptomatic treatment, if necessary, hemodialysis or peritoneal dialysis treatment, but this is only an auxiliary measure, is not the key to treatment. To summarize the treatment process of kidney failure can be divided into four parts, as follows: 1, treatment of chronic renal failure, the first is the treatment of the cause of the cause of the cause of the treatment of kidney failure from the "source". The cause of kidney failure is due to various causes of deformation and damage to the intrinsic cells of the kidney. Take glomerular renal failure as an example, we can explain our treatment method: glomerular disease is an immune disease, its pathogenesis is often triggered by antigen or antibody binding to form immune complexes, and deposited in the glomerulus (immune complexes). With the involvement of inflammatory mediators (e.g., complement, interleukins, reactive oxygen species, etc.), it finally leads to glomerular injury. In therapeutic practice, the following measures are taken: 1. Dilate renal arteries to increase the effective perfusion of glomeruli, tubules and interstitium, accelerate the supply of damaged cells i, and relieve their hypoxic state. 2.Dilate the systemic arteries to reduce and relieve the systemic hypertensive state, especially to reduce the glomerular intra-glomerular pressure and reduce the glomerular hypercritical state. 3.By accelerating the supply, avoiding the endothelial cells from being activated to inhibit the formation of microchemical tethering. 4.Inhibit the chemotaxis and infiltration of a series of inflammatory factors by accelerating the blood velocity and through adequate supply to stop the abnormal release of already activated inflammatory cells. Clinical observation reality, through the implementation of the above four treatment measures, the normal metabolic function of the glomerulus is activated, when the glomerular condition improves, the function of the whole kidney also improves 2, treatment of chronic renal failure, followed by treatment for the pathogenic process The development process of chronic renal failure, which is the gradual reduction of effective kidney units, the process of continuous loss of kidney function. In this process, both kidneys gradually atrophy, a large number of glomerulosclerosis, tubular-interstitial fibrosis. Therefore, the process of renal failure is also the process of deepening renal fibrosis. Interrupting the process of renal fibrosis is important to effectively control the progression of the disease to uremia. Although some scientific research institutions have pointed out that some Chinese medicines are effective in blocking the process of renal fibrosis, not many of them are really applied to clinical practice. The drugs used in our hospital are a series of Chinese medicines that have been micronized. The activity of Chinese medicine increases after micronization treatment, and many drug components that are difficult to function under traditional conditions can also function adequately. 3.Treatment of chronic renal failure, once again, is the treatment for symptoms Most of the clinical symptoms of chronic renal failure patients are related to the imbalance of water-electrolyte and acid-base balance; other renal failure symptoms are related to uremic toxins. Symptom-specific treatment can improve the disorder of internal environment, regulate the imbalance of renal balance, and improve the quality of life of kidney failure patients. Microchemical Chinese medicine infiltration therapy in the treatment of renal failure, the specific approaches are: 1. Treatment for renal anemia, one of the common symptoms of renal failure, by using recombinant human erythropoietin (Rhepo, hereinafter referred to as EPO), the active substance of Chinese medicine, to treat renal anemia. Clinical observation shows that the effect is very significant. This therapy is universally applied to patients with anemia. In general, renal failure patients, especially maintenance hemodialysis patients, lose small amounts of blood over a long period of time, which causes the loss of some hematopoietic materials, such as iron and folic acid. In order to make EPO fully effective, some hematopoietic raw materials should be replenished before using EPO. the active substance of Chinese medicine is rich in more than ten kinds of trace elements, including iron and folic acid, which can fully meet the need of improving anemia condition. 2, for the treatment of hypertension in renal failure Hypertension is a reversible condition, for this reason we pay great attention to grasp this link in the treatment of chronic renal failure. The long-term tightening state of renal blood vessels is the key cause of renal hypertension, so the most important and effective means of treating hypertension is direct vasodilation. We found in the clinical process that there are a large number of vasodilating factors in the microprocessed Chinese medicine play a synergistic role to make the blood vessels become relaxed, so it relieves the renal hypertension caused by insufficient diastole and excessive tension of blood vessels, and strongly relieves the symptoms of kidney failure patients. 4.Treatment for the recovery of renal function in patients with chronic renal failure Through the treatment for the cause, pathogenesis and symptoms, the condition can be effectively relieved and controlled, but for patients with renal failure, just controlling the condition is not enough. Because a large number of kidney units in the body of kidney failure patients are damaged and fibrosis or sclerosis, both kidneys or single kidney atrophy, especially in the uremic period, only about 10% of the remaining kidney units, if you can not repair the thousands of necrotic kidney units, the remaining kidney units are still "overload" work, over time, inevitably Inevitably, lesions will also appear. This is the reason why many patients are not cured for a long time and their condition is recurrent. The only effective way to get to the root of the problem is to repair the damaged kidney units so that they can regain their metabolic capacity. Health Tips Diet: 1. The focus of dietary treatment is to limit protein intake to reduce nitrogen retention. However, care should be taken to ensure adequate calories and sufficient essential amino acids. The amount of protein intake for each patient should be flexible according to its muscle research clearance rate. 2, adhere to a high quality low protein diet, low phosphorus, low salt, high calories; avoid aggravating factors, moderate cold, avoid wind and cold; avoid external sensation, infection, diet with moderation. Prevention: 1, to avoid overwork and strong mental stimulation; 2, prevention of infection, remove the foci of infection to reduce the cause of deterioration 3, have a habit of smoking and alcohol should be quit; 4, with swelling, hypertension, proteinuria significant and a little action is aggravated by the symptoms, are recommended to bed rest. Note: 1. Take good care of the mouth to reduce irritation and prevent mouth ulcers, which may affect eating. 2, the patient has headache, insomnia, irritability, the room light should be dark, in order to facilitate the patient to rest, if necessary, use sedatives, can take Valium, etc. 3, high blood pressure, blood pressure should be measured regularly, according to the condition with antihypertensive drugs, and adhere to the regular intake. 4.When there is bleeding, use hemostatic drugs according to the doctor's request. 5. Pay attention to the protection of the skin to prevent abrasions and bedsores. 6.If the condition is serious, send to hospital for hemodialysis or peritoneal dialysis treatment in time. Chronic renal failure patients contraindications A. Prevent over-supplementation. Chinese medicine says "deficiency is tonic, the real is diarrhea", we should follow the principle of "no deficiency is not tonic", "what is lacking is tonic", for the lack of body, can be tonic, but must be tonic in moderation. Otherwise, it will cause imbalance of yin and yang in human body. At the same time, you should know that medicine is not as good as food, medicine is three points of poison, can use food supplementation, do not use medicine to supplement. Second, to prevent excess heat energy. Some chronic renal failure patients have a big appetite in autumn, often resulting in excess caloric intake, fat accumulation, and start "autumn fat". Because obesity can bring many diseases, so patients with chronic renal failure should not indulge their appetite in the autumn diet and pay attention to moderation. Third, pay attention to balanced nutrition. According to the Dietary Guidelines for Chinese Residents, food should be varied, with cereals as the mainstay, and coarse and fine foods. A single food cannot supply the body with comprehensive nutrition, such as cereals mainly supply calories and vitamin B1; beans and soy products mainly supply plant protein; vegetables and fruits mainly supply vitamin C, inorganic salts and dietary fiber; animal food mainly supplies high-quality protein, fat, vitamins, etc. Fourth, avoid digestive tract diseases. Autumn weather from hot to cool, the human body in order to adapt to this change, physiological metabolism has also changed. The ancient doctors of China put forward the idea of "autumn should be warm", that is to say, chronic renal failure patients should avoid eating cold food in autumn, should eat more warm food, so as to help protect the gastrointestinal, to prevent diarrhea, dysentery, loose stools and other gastrointestinal diseases. In addition to diet, chronic renal failure patients must be under the guidance of a specialist in the standardization of medication, the principle of medication is: less and more precise, to safe and effective prevail. It is important to go to a regular hospital and use medication under the guidance of a specialist. All kinds of advertisements, clinics and charity clinics should be treated calmly, and it is better not to use them. [1] Related information Uremic toxic substances: generally divided into small molecules (molecular weight <500dal), medium molecules (molecular weight 500￣5000dal) and large molecules (molecular weight〉5000dal) three categories. Large molecule toxic substances, the most from the attention of the urea, guanidine. A large molecule substances (1) urea: uremia, the largest content of a metabolite in the body fluid. When its serum concentration is quite high, it can cause headache, weakness, nausea, vomiting, drowsiness, bleeding tendency, etc. The toxicity of urea is related to the length of its existence, and its metabolite cyanate can cause carbamylation of proteins, which has an important relationship with the symptoms of uremia. (2) guanidine: guanidine is a metabolite of certain amino acids and creatinine, injecting animals with large amounts of methylguanidine, a series of symptoms similar to uremic syndrome can occur. Methylguanidine is positively charged and easily binds to negatively charged phospholipids in cells, accumulates in cells and forms cytotoxicity. The level of methylguanidine production is parallel to creatinine. Both plasma methylguanidine and urinary methylguanidine rise when the urine volume is less than 400 ml/d. Guanosuccinic acid is less toxic than methylguanidine and is excreted in the urine of normal people at about 10 mg per day, which can increase fivefold in uremia. The effects of guanidinosuccinic acid are: ① Inhibit the adhesion and aggregation of platelets, and have an inhibitory effect on platelet factor III. ②Promote autohemolysis. ③Inhibit lymphocyte function. ④ Causes impairment of enzyme activity in brain tissue. (3) Amines: including fatty cyclamines, aromatic cyclamines and polyamines. High concentration of fatty amines (1-methylamine, 2-methylamine, 3-methylamine, etc.) can cause myoclonus, fluttering tremor and hemolysis, and can also inhibit the activity of certain enzymes. Aromatic spinamines (amphetamines, tyramine) have inhibitory effects on brain tissue chlorination process, succinate oxidation and dopa carboxylase activity. Polyamines include spermidine, sperm, putrescine and cadaverine. High concentration of polyamines can cause anorexia, nausea, vomiting and proteinuria, and can promote erythrocyte lysis, inhibit erythropoietin production, inhibit Na+-ATPase and Mg2+-ATPase activities, and also increase the permeability of microcirculation, promote the production of uremic lung, acute pulmonary edema, ascites and cerebral edema. Second, medium molecular substances The application of chromatography and other techniques confirmed that 8 to 9 clear peaks can be found in the plasma of uremic patients, and in severe patients, peak number 7 is particularly pronounced. The peritoneal clearance of urea is about 4 to 6 times lower than that of artificial membranes for hemodialysis, but the peritoneal clearance of medium-molecular substances is higher than that of artificial membranes. Although the rate of decline in urea nitrogen was slower in peritoneal dialysis patients, the relief of neurological symptoms was superior to that of hemodialysis, supporting the view that medium-molecular substances are toxicogenic. The medium-molecule toxicants may include: ① high concentrations of normal metabolites. (2) Hormones with normal structure and increased concentration. (3) Peptides produced by disorders of cellular metabolism. ④Cellular or bacterial lysis products. High-depth middle-molecule substances can cause peripheral neuropathy, uremic encephalopathy, inhibition of erythropoiesis, inhibition of insulin activity, inhibition of antibody production, impairment of platelet function, low cellular immune function, sexual dysfunction and atrophy of exocrine glands. Third, the role of PTH Uremic patients often have secondary parathyroid hyperplasia and elevated levels of parathyroid hormone (PTH) in the blood. The causes may be due to elevated blood phosphorus; resistance of bone to the calcifying effects of PTH; and altered vitamin D metabolism. Elevated PTH levels can cause multi-organ damage, increase intracellular calcium concentrations, alter the ratio of intracellular to extracellular calcium, affect cell membrane permeability, promote soft tissue calcification, and increase the accumulation of protein metabolism nitrogen in the blood. (1) EEG is altered by elevated PTH. Motor nerve conduction velocity is slowed. Increased Ca2+ content in the brain. (2) Elevated PTH levels are an important cause of anemia. The main pathway is that PTH inhibits erythropoiesis, reduces erythrocyte survival, and causes bone calcium freeing and bone marrow fibrosis. (3) Effects of PTH on the myocardium. The heart is one of the important target organs of PTH, which can affect cardiac function and cardiomyocyte metabolism. Principles of medication for renal failure 1, early mild cases available A, and pay attention to control fluid intake, supplement vitamins and energy, maintain electrolyte and acid-base balance; 2, severe cases should be timely, early dialysis treatment, dialysis can choose peritoneal dialysis maximum protection of residual kidney function; pay attention to complications such as hypertension, anemia, proteinuria,,, etc., try to correct the damage to the kidneys by reversible factors; if necessary, daily dialysis In case of combined infection, use drugs in item C; 4. In case of combined hypertension, use drugs in item A or item C; 5. In case of combined heart failure, use cardiac drugs such as Cediran; 6. Chronic renal failure is easily misdiagnosed Mr. Wu has been suffering from "gastritis" for 5 years, and after the Spring Festival, he suddenly had gastric bleeding again, and his condition did not improve significantly after treatment, but still bleeding intermittently. The Zhengzhou hospital did a systematic examination for him and found that Mr. Wu was suffering from chronic renal failure. Chronic renal failure is a serious disease that affects multiple systems throughout the body, and sometimes, it is easy to misdiagnose because the symptoms of a system are particularly prominent. Why does the digestive system appear abnormal when you are suffering from kidney disease? This is because when the kidney function is damaged, the toxin discharge in the urine is reduced, the toxin in the blood will increase, and the toxin discharge from the digestive tract will also increase. The mucosa of the digestive tract is stimulated by the toxin, which causes superficial inflammation and ulcers in the mucosa of the stomach and duodenum, and even causes hemorrhage in the upper gastrointestinal tract. Clinically, it is often seen that patients with chronic renal failure see gastroenterology for a long time, and gastroscopy does have lesions, unbeknownst to them, which is one of the complications of chronic renal failure. In the early stage of chronic renal failure, most patients have no symptoms and blood abnormalities are not obvious, only manifesting as hypertension, proteinuria and mild elevation of serum uric acid level. Wu Xianming reminds that it is important to keep a close eye on these suspicious conditions to avoid misdiagnosis. The only way to detect kidney failure early is to do kidney function tests. For GI reactions due to kidney disease, the most important thing should be timely treatment of kidney failure. Gastrointestinal symptoms that have appeared should be closely observed and patients should be advised to eat easily digestible and non-irritating food. Patients with loss of appetite, nausea and vomiting should be put on bed rest. What are the treatment measures for pediatric chronic renal failure? The management of pediatric chronic renal failure requires monitoring of the pediatric clinical (physical examination and blood pressure) and laboratory tests including hemoglobin, electrolytes (hyponatremia, hyperkalemia, acidosis), blood urea nitrogen and creatinine measurements, calcium and phosphorus levels, and alkaline phosphatase activity. Parathyroid endocrine levels and bone X-rays should be checked regularly for early detection of osteotropic disorders. Chest radiographs and cardiac ultrasound may be useful in understanding cardiac function. Nutritional status can be monitored by regular checks of serum albumin, zinc, iron conversion, folic acid and iron levels. 1, the diet of chronic renal failure when the pediatric glomerular filtration to less than 50% of normal, pediatric growth rate decreases, the main reason for this has insufficient intake of calories. Although it is not known what the appropriate caloric intake is when renal insufficiency is present, it is important to make the caloric intake comparable or higher than the age group of the child if possible. Dietary caloric intake can be increased with unrestricted carbohydrates such as sugar, jam, bee dense, glucose polymers, and fats such as medium chain triglyceride oil, provided the patient can tolerate them. When urea nitrogen is above 30 mmol/L (80 mg/dl) the patient may experience nausea, vomiting and anorexia, which may be relieved by restricting protein intake. Because children in renal failure still need a certain amount of protein for growth, so give protein 1.5g/(kg・d), and should be given high-quality protein (eggs and lean meat) containing a large amount of essential amino acids, such as eggs, milk, followed by meat, fish, chicken and poultry. Milk is too high in phosphorus and should not be used more than necessary. Food such as glucose and peanut oil should be used to supplement calories. Due to insufficient intake or dialysis loss, children with renal insufficiency may have water-soluble vitamin deficiency and must be routinely supplemented. If there is a deficiency of iron, zinc and other trace elements must also be supplied, fat-soluble vitamins such as A, E and K do not need to be supplemented. 2, water and electrolyte treatment of pediatric renal insufficiency, rare to limit the amount of intake, because there and brain "thirst center" to regulate, unless the development of end-stage renal failure, then need to use dialysis. In the vast majority of children with renal insufficiency, a normal sodium balance can be maintained with an appropriate diet. In some patients with renal insufficiency due to anatomical abnormalities, if a large amount of sodium is lost by urine, the sodium must be supplemented by diet; conversely, if the patient has hypertension, edema or congestive heart failure, the sodium must be restricted, sometimes in combination with tachyphylaxis, 1-4 mg/(kg/24h). If renal function deteriorates further, dialysis treatment is required. Hyperkalemia can be treated with dietary potassium control and oral alkaline or potassium reducing resin (sodium polystyrene sulfonate, Kayexalate). Pediatric renal insufficiency almost always has acidosis, which generally does not require treatment, unless serum bicarbonate is below 20 mmol/L, which must be corrected with sodium bicarbonate. 3, renal osteodystrophy is often complicated by renal osteodystrophy when there is hyperphosphatemia, hypocalcemia, increased parathyroid endocrine levels and increased serum alkaline phosphatase activity. Serum phosphorus levels generally rise when the glomerular filtration rate falls below 30% of normal. Serum calcium decreases secondary to hyperparathyroidism. Hyperphosphatemia can be controlled with a diet low in phosphorus, or with calcium bicarbonate or antacids taken orally to promote phosphorus excretion from the intestine. Aluminum toxicity is also a concern in the pediatric population and serum aluminum levels must be monitored regularly. In severe renal insufficiency and vitamin D (Vit. D) deficiency, Vit. D is used for persistent low blood calcium, rickets on X-ray and increased serum alkaline phosphatase activity. 4, anemia most patients with hemoglobin stable at 60-90g/L (6-9g/dl) do not need blood transfusion, if hemoglobin is below 60g/L then carefully input red blood cells 10ml/kg (small amount can reduce the risk of blood circulation overload.) . 5, hypertension to hypertensive emergencies can be sublingual nifedipine or through the intravenous injection of diazoxide that is hypotensive zine (5mg/kg, extreme amount of 300mg, in 10 seconds injection). In severe hypertension complicated by blood circulation overload, tachyphylaxis (2-4mg/kg at a rate of 4mg/min) can be given. In case of renal insufficiency, sodium nitroprusside must be applied with caution, as thiocyanate may accumulate. In short, we should strive for early diagnosis and removal of the cause, if found too late, although the cause is removed, the damage to the kidney tissue is difficult to recover. If the cause is urinary tract obstruction, appropriate surgical treatment should be done, but the child is often in poor renal function and cannot tolerate too much surgery, so nephrostomy or suprapubic cystostomy can be done first to facilitate drainage. If there is persistent or intermittent pyuria, the infection should be actively controlled and followed up and reviewed. For patients with end-stage renal disease or difficult-to-recover renal failure, chronic hemodialysis (artificial kidney, also known as long-term intermittent hemodialysis) has been applied in recent years, enabling many patients to continue to survive or return to normal life. The current long-term regular dialysis, usually 2 to 3 times a week, can be performed at night while sleeping. In children treated with chronic hemodialysis, the development of secondary sexual characteristics and weight gain are not significantly affected, and only height is slightly affected. In recent years, the implementation of chronic hemodialysis has been transferred from hospitals to patients' homes in foreign countries, and the duration of dialysis in children has been as long as 4 to 5 years. Peritoneal dialysis has also been used for chronic renal failure, mainly in the intraperitoneal cavity with a long-term fixed catheter and daily dialysis on a regular basis, and can also be performed in the home according to medical advice. The ultimate goal of pediatric end-stage renal failure treatment is kidney transplantation. In foreign countries, the success rate of kidney transplantation in children over 5 years of age is the same as that of adults, and effective chronic hemodialysis is required prior to kidney transplantation (to keep the child alive while waiting for a suitable donor kidney) or after rejection.