Chronic renal failure (CRF) refers to a series of symptoms and metabolic disorders caused by various kidney diseases, which lead to gradual irreversible decline of renal function until functional loss, and is called chronic renal failure for short. The end stage of chronic renal failure is uremia, which people often say. Uremia is not an independent disease, but a clinical syndrome of various advanced kidney diseases, which is a syndrome composed of a series of clinical manifestations when chronic renal failure enters the terminal stage. Metabolic acidosis and imbalance of water and electrolyte are the most common clinical manifestations. (1) Metabolic acidosis In uremia stage of chronic renal failure, acidic products of human metabolism such as phosphoric acid and sulfuric acid are retained due to renal excretion disorder, which may lead to "uremic acidosis". In mild chronic acidosis, most patients have fewer symptoms, but such as arterial blood HCO 3 <: 15 mmol/L, obvious loss of appetite, vomiting, weakness, deep breathing and so on may occur. (2) Water and sodium metabolism disorder, mainly manifested as water and sodium retention, or hypovolemia and hyponatremia. When renal function is not complete, the adaptability of the kidney to excessive sodium load or excessive volume gradually decreases. Patients with uremia who restrict water inappropriately may lead to excessive volume load, common subcutaneous edema (eyelids, lower limbs) or/and body cavity effusion (chest cavity and abdominal cavity) in different degrees. At this time, it is easy to have high blood pressure, left ventricular dysfunction (manifested as chest tightness, decreased activity tolerance and even inability to lie down at night) and brain edema. On the other hand, when the patient has a lot of urine, and the water is excessively restricted, or the digestive tract symptoms such as vomiting and diarrhea are complicated, it is easy to cause dehydration. Clinically, it is more common to have excessive volume load, so uremia patients should pay attention to properly controlling water intake (including soup, porridge, fruit and other water-rich foods besides drinking water), and avoid excessive rehydration during diagnosis and treatment to prevent heart failure and pulmonary edema. (3) potassium metabolism disorder: when GFR is reduced to 20-25ml/min or lower, the ability of renal potassium excretion gradually decreases, and hyperkalemia is easy to occur at this time; Especially when excessive potassium intake, acidosis, infection, trauma and gastrointestinal bleeding occur, hyperkalemia is more likely to occur. Severe hyperkalemia (serum potassium >; 6.5 mmol/L) is dangerous and needs timely treatment and rescue (see treatment of hyperkalemia). Sometimes hypokalemia can also occur due to insufficient potassium intake, excessive gastrointestinal loss, application of potassium-expelling diuretics and other factors. Hyperkalemia is common in clinic, so uremia patients should strictly limit the intake of foods with high potassium content and check their blood potassium regularly. (4) calcium and phosphorus metabolism disorder, mainly manifested as excessive phosphorus and calcium deficiency. In chronic renal failure, renal production 1, 25-(OH) 2d3 decreased, which reduced the absorption of calcium in intestine. Target organs are resistant to 1, 25-(OH) 2d3, which reduces the calcium reabsorption of renal tubules. In addition, hyperphosphatemia can increase the product of calcium and phosphorus, promote the deposition of calcium phosphate, and cause ectopic calcification and decrease of blood calcium. Food is rich in phosphorus, and the blood phosphorus concentration is regulated by the absorption of phosphorus by intestine and the excretion of kidney. When glomerular filtration rate decreased and urinary phosphorus excretion decreased, blood phosphorus concentration gradually increased, and high blood phosphorus further inhibited the synthesis of 1, 25-(OH) 2d3, which aggravated hypocalcemia. Parathyroid gland secretes more PTH to maintain blood calcium. It leads to secondary hyperparathyroidism (referred to as hyperparathyroidism). Protein, Metabolic Disorders of Sugar, Fat and Vitamins The metabolic disorder of protein in CRF patients is generally manifested as the accumulation of protein metabolites (azotemia), including urea, guanidine compounds, creatinine, amines, indoles, phenols and middle molecular substances. Urea is excreted through the kidney and accumulated in uremia, which may be related to fatigue, anorexia, vomiting, inattention, hypothermia and bleeding tendency. Under normal circumstances, arginine is mainly metabolized into urea, guanidinoacetic acid and creatinine in the liver, and urea and creatinine accumulate in uremia, while arginine can be decomposed into methylguanidine and guanidino arginine by other ways. Among them, methylguanidine is the most toxic small molecular substance, and its accumulation in the body can reach 70 ~ 80 times of the normal value, which is related to many clinical symptoms such as weight loss, shortened life span of red blood cells, vomiting, diarrhea, drowsiness and so on. Amine aliphatic amines can cause myoclonus, flapping-wing tremor and hemolysis; Polyamines (spermine, cadaverine, putrescine) can cause anorexia, nausea, vomiting and proteinuria, and can promote erythrocyte lysis, inhibit the production of erythropoietin, and promote the occurrence of pulmonary edema, ascites and brain edema in renal failure. Abnormal glucose metabolism is mainly manifested in impaired glucose tolerance and hypoglycemia, the former is more common and the latter is rare. Hyperlipidemia is quite common, in which most patients show mild to moderate hypertriglyceridemia, a few patients show mild hypercholesterolemia, or both. The disorder of vitamin metabolism is quite common, such as the increase of serum vitamin A level, vitamin B6 and folic acid deficiency. Cardiovascular disease is one of the main complications and the most common cause of death in CKD patients. Especially in the stage of end-stage renal disease (uremia), the mortality rate of cardiovascular diseases has further increased (accounting for 45%-60% of uremia deaths). Recent studies have found that cardiovascular adverse events and atherosclerotic cardiovascular diseases in uremia patients are about 15-20 times higher than those in the general population. Chronic renal failure patients may have heart failure, arrhythmia and myocardial damage due to renal hypertension, acidosis, hyperkalemia, sodium and water retention, anemia and toxic substances, etc. Due to the stimulation of urea (and possibly uric acid), aseptic pericarditis may also occur, and patients may have pain in the precordial area, and they may smell pericardial rubbing sound during physical examination. In severe cases, cellulose and bloody exudates appear in the pericardial cavity. Vascular calcification and atherosclerosis also play an important role in cardiovascular diseases. The gas exhaled by patients with respiratory symptoms smells like urine, which is because bacteria decompose urea in saliva to form ammonia; Shortness of breath and shortness of breath may occur when there is too much body fluid; Patients with acidosis breathe slowly and deeply. In severe cases, the particularity of acidosis can be seen: Kussmaul breathing (deep breathing). Excessive body fluids and cardiac insufficiency can cause pulmonary edema or pleural effusion; The increase of alveolar capillary permeability and pulmonary congestion induced by uremic toxin can cause "uremic pulmonary edema". At this time, the "butterfly wing" sign can appear in lung X-ray examination, and the above symptoms can be quickly improved by timely diuresis or dialysis. Cellulose pleurisy is inflammation caused by urea stimulation; Pulmonary calcification is caused by the deposition of calcium phosphate in lung tissue. Gastrointestinal symptoms The earliest symptoms of digestive system in uremia patients are anorexia or indigestion, and anorexia, nausea, vomiting or diarrhea may occur when the condition worsens. The occurrence of these symptoms may be related to the decomposition of urea into ammonia by urease of intestinal bacteria, and the irritation of ammonia to gastrointestinal mucosa causes inflammation and multiple superficial small ulcers. In addition, nausea and vomiting are also related to the dysfunction of the central nervous system. Gastrointestinal bleeding is also common, and its incidence is significantly higher than that of normal people, mostly due to gastric mucosal erosion or peptic ulcer. Blood system manifestations The abnormal blood system of CRF patients is mainly characterized by renal anemia and bleeding tendency. Most patients generally have mild and moderate anemia, which is mainly due to the lack of erythropoietin, so it is called renal anemia; If accompanied by iron deficiency, malnutrition, bleeding and other factors, can aggravate the degree of anemia. Patients with advanced CRF have abnormal platelet function and tend to bleed, such as subcutaneous or mucosal bleeding spots, ecchymosis, gastrointestinal bleeding, cerebral hemorrhage and so on. Early symptoms of neuromuscular system may include insomnia, inattention, memory loss, etc. In uremia, there may be apathy, delirium, convulsion, hallucination, coma and mental abnormality. Peripheral neuropathy is also very common, and sensory nerve disorder is more obvious. The most common is the loss of sensation in the sock-like distribution of extremities, numbness, burning or pain in limbs, dullness or disappearance of deep reflexes, and increased neuromuscular excitability, such as muscle tremor, spasm and restless leg syndrome. The occurrence of these symptoms is related to the following factors: ① The accumulation of some toxic substances may cause degeneration of nerve cells; (2) electrolyte and acid-base balance disorder; ③ Cerebral vasospasm, hypoxia and increased capillary permeability caused by renal hypertension can cause degeneration of brain nerve cells and brain edema. Dialysis imbalance syndrome may occur in the first dialysis patients, with nausea, vomiting, headache, convulsion, etc., which is mainly caused by the imbalance of osmotic pressure of intracellular and extracellular fluids, brain edema and increased intracranial pressure after hemodialysis. Bone pathological changes Renal osteodystrophy (i.e. renal osteopathy) is quite common, including fibrocystic osteitis (high turnover osteopathy), adynamic bone disease, osteomalacia (low turnover osteopathy) and osteoporosis. Before dialysis, about 35% of the patients found abnormal bone X-ray, but bone pain, walking inconvenience and spontaneous fracture were quite rare (less than 10%). However, about 90% of bone biopsy can find abnormalities, so early diagnosis depends on bone biopsy. Fibrocystic osteitis is mainly caused by high PTH, which is prone to bone salt dissolution and rib fracture. X-ray examination shows cystic defects of bones (such as phalanges and ribs) and osteoporosis (such as spine, pelvis and femur). The occurrence of osteogenesis is mainly related to the relatively low blood PTH concentration and the lack of some osteogenic factors, which is not enough to maintain bone regeneration. If dialysis patients use active vitamin D, calcium and other drugs excessively for a long time, or the calcium content in dialysate is high, the blood PTH concentration may be relatively low. Diagnosis and differential diagnosis of uremia is not an independent disease, but a group of clinical syndromes. In the final stage of chronic renal failure, the three major functions of the kidney are lost, and a series of symptoms and metabolic disorders appear, thus forming uremia. The diagnosis of uremia depends not only on the level of serum creatinine, but also on the clinical manifestations of the above systems. In the early stage of chronic renal insufficiency, there are only symptoms of primary disease in clinic, and the creatinine clearance rate can only be seen in the examination. These patients with uremia in compensatory stage often suffer from sudden deterioration of renal function and uremia symptoms (that is, the clinical manifestations of various systems mentioned above), which are clinically called reversible uremia, but once the stress factors are removed, renal function can often return to compensatory stage. If the condition develops to the point that the "healthy nephron" can't meet the minimum requirements of the body, uremia will gradually show up even without stress factors. The damage of all the above uremic systems may not be manifested. In different patients, the symptoms of uremia may be different, and the time when the symptoms of each system occur is not the same. Auxiliary examination 1. Blood routine examination in uremia, the hemoglobin is generally below 80g/L, and most of them are only 40 ~ 60g/L, which is normal cell eupigmentary anemia. When the patient is complicated with chronic blood loss and malnutrition, it can also be manifested as small cell hypochromic anemia. There are few changes in white blood cells, which can increase the number of white blood cells in acidosis and infection. The platelet count is low or normal, but the function is reduced, and the erythrocyte sedimentation rate is often accelerated due to anemia and hypoproteinemia. 2. Urine routine examination shows that the urine changes of uremia patients are quite different with different primary diseases. The * * * similarities are as follows: ① urine osmotic pressure is reduced, and most morning urine is below 450mOsm/kg, and the specific gravity is low, mostly below 1.0 18, and it is fixed at1.01.0 in severe cases. During the concentration and dilution test, the nocturnal urine volume is greater than the daily urine volume, and the urine specific gravity of each time does not exceed 1.020, and the difference between the highest and lowest urine specific gravity is less than 0.008. ② The urine volume decreases, mostly below 1000ml/ day. When the creatinine clearance rate drops to below1.0 ~ 2.0 ml/second in the late stage, there is no urine. ③ The urinary protein is+~+++,but in the late stage, because most of the glomeruli have been destroyed, the urinary protein is reduced. ④ Urine sediment examination can include a number of red blood cells, white blood cells, epithelial cells and granular casts. If a wax-like cast with thick, short, homogeneous and cracked edges can be found, it is meaningful for diagnosis. 3. Renal function examination In the compensatory period of renal insufficiency, although the renal creatinine clearance rate decreased, the serum creatinine did not increase; In azotemia's stage, although serum creatinine has increased, the patient has no clinical symptoms of uremia and metabolic acidosis. In uremia, when renal creatinine clearance rate <: At 25ml/min, serum creatinine will increase obviously, accompanied by metabolic acidosis. 4. Blood biochemical examination shows that plasma protein is decreased, and the total protein is often below 60g/L, among which albumin is often obviously decreased, mostly below 30g/L.. Blood calcium is low, often around 2mmol/L, and blood phosphorus is mostly higher than1.7 mmol/L. Blood potassium and blood sodium depend on the condition. 5. Other examinations (1)X-ray examination: Uremic patients can have abdominal X-ray examination to observe the size and shape of the kidney and whether there are stones in the urinary system. Abdominal lateral radiograph can show whether there is atherosclerosis or not. In severe renal insufficiency, because of the poor function of renal excretion contrast agent, it is not developed after injection of contrast agent, so it is generally not suitable for contrast examination. (2) Radionuclide renogram and renal scanning examination are helpful to understand the size, blood flow, secretion and excretion functions of both kidneys. (3) Renal ultrasound and CT are helpful to determine the location, size and thickness of the kidney and whether there are hydrops, stones and tumors in the renal pelvis. Under normal circumstances, uremia patients' kidneys atrophy and their cortex becomes thinner. However, the kidneys of uremia patients caused by diabetes, lupus, vasculitis and other secondary causes can not be significantly reduced, but the cortical echo is enhanced under B-ultrasound. Ultrasound examination of kidney has the advantages of economy, convenience, non-invasion, rapidity, etc. It can judge the size of kidney, cortical echo, etc., and is widely used in clinic. Treatment of chronic renal insufficiency requires renal replacement therapy when it progresses to uremia. Often, some patients have entered uremia stage, but they have been procrastinating, unwilling to receive dialysis treatment, and always worried about the side effects and costs of dialysis. Many patients will also hope that Chinese medicine treatment can "cure" uremia and get rid of dialysis. In fact, dialysis is to replace the kidney. When the patient enters uremia, the patient's kidney should be damaged by more than 90%. If the alternative treatment is delayed at this time, the toxin will remain in the body and will also bring irreversible damage to other organs of the body, such as the heart, digestive system, bones and blood system. Uremia is a disease that cannot be cured by drug treatment, and there is no so-called "panacea" that can cure uremia. Therefore, uremia patients should not hesitate to take renal replacement therapy in time, that is, dialysis treatment. For uremia patients whose condition is relatively stable, the condition of such patients is relatively stable. Although renal replacement therapy needs to be started as soon as possible, there is no indication of emergency dialysis. Such patients should actively prepare for dialysis while taking medication and controlling diet. For example, medical staff should educate patients about the relevant contents before dialysis, so that patients can fully understand the necessity and limitations of renal replacement therapy, and choose the appropriate dialysis method (hemodialysis or peritoneal dialysis) according to their own conditions, family environment, work situation and economic situation; Patients who plan to undergo hemodialysis need to undergo colostomy1~ 3 months in advance, and contact the hemodialysis center for long-term dialysis treatment. For patients who are preparing for peritoneal dialysis, the peritoneal dialysis tube should be inserted 2 ~ 4 weeks in advance. The common uremia emergencies include: hyperkalemia, uremia, the decrease of renal potassium excretion ability, and hyperkalemia is prone to occur at this time; Especially when excessive potassium intake, acidosis, infection, trauma and gastrointestinal bleeding occur, hyperkalemia is more likely to occur. Severe hyperkalemia (serum potassium >; 6.5 mmol/L) may lead to cardiac arrest, which is life-threatening, so it needs to be rescued in time: ① Calcium is used to resist the toxicity of high potassium to myocardium, and the same amount of hypertonic glucose is usually added to10 ~ 20 ml, and it is slowly pushed statically for at least 5 minutes. If the arrhythmia does not improve after 5 minutes of injection or recurs soon after effective, it can be injected again; Sodium lactate or sodium bicarbonate can promote potassium ions to enter cells, antagonize the inhibition of potassium on the heart and increase the excretion of potassium in urine; ③ The combined application of glucose and insulin (4g glucose: 1U insulin) can promote the transfer of potassium into cells; ④ Oral or injection of diuretics (furosemide, torasemide, etc.) to promote renal potassium excretion; ⑤ Oral cation exchange resin can promote potassium excretion from intestine; ⑥ High potassium is very serious (> 6.5mmol/l), and when the above treatment effect is not good, hemodialysis can be used to reduce blood potassium. In uremia patients with heart failure and pulmonary edema, the function of regulating water and sodium balance of kidney is decreased or even lost, and the urine volume is reduced, which is easy to form overload of capacity. In severe cases, heart failure and pulmonary edema occur, which is life-threatening. The preventive and therapeutic measures include: ① controlling water intake, making the water inflow less than the water outflow, and giving diuretics when necessary; ② Hemodialysis, ultrafiltration and dehydration; ③ Cardiotonic therapy, tube dilatation and other treatments. Metabolic acidosis blood pH <: 7.2, carbon dioxide binding force <; 13mmol/l, with clinical manifestations of metabolic acidosis (loss of appetite, vomiting, weakness, deep breathing, etc.). Treatment measures: ① intravenous sodium bicarbonate: 5% sodium bicarbonate solution intravenous drip; ② Hemodialysis corrects acid-base balance disorder. Toxin level is high, blood creatinine ≥707umol/l and urea nitrogen ≥ 28.6 mmol/L. When uremia symptoms are obvious, emergency hemodialysis is needed to remove toxins. When serious complications such as pericarditis and gastrointestinal bleeding occur. When the above situation requires emergency dialysis treatment, it is necessary to establish a blood flow path through central venous intubation. The dialysis imbalance syndrome may occur in the first dialysis patient, so the first dialysis time is short, generally about 2 hours. Hemodialysis and Peritoneal Dialysis Hemodialysis: The patient's blood is introduced into the dialysis machine through blood vessels, and the material exchange between dialysis membrane and dialysate is carried out in the dialysis machine, and then the purified blood is returned to the body, so as to achieve the purpose of discharging waste, correcting electrolyte and acid-base balance disorder. Many patients can survive10 ~ 20 years if they insist on reasonable dialysis for a long time. Hemodialysis needs to go to the hospital twice or three times a week, each time for about 4 hours. Its advantage is that there is less waste accumulated in the body after hemodialysis, and it has a fixed time to go back to the hospital for treatment every week. If the condition changes, it can be treated in time. There are professional medical personnel to operate during dialysis, so it is not necessary to do it yourself. The disadvantages are also obvious: needles need to be inserted every time; Anemia is more serious; Blood pressure will be affected before and after dialysis, which is unfavorable to patients with cardiovascular disease and diabetes. Need to strictly control diet; It is easy to feel uncomfortable before dialysis; Cannot arbitrarily change the dialysis time; The risk of infection with hepatitis B and hepatitis C is greatly increased. Peritoneal dialysis: a special liquid called "peritoneal dialysis solution" is poured into the abdominal cavity through a "peritoneal dialysis tube". At this time, one side of the peritoneum is blood containing metabolic waste and excess water, and the other side is dry peritoneal dialysis solution, so the metabolic waste and excess water in the blood will run into the peritoneal dialysis solution through the peritoneum. Keep it for 3-4 hours (it can be kept for 8- 10 hour at night), then release these waste-containing peritoneal dialysate from the abdominal cavity and pour in new peritoneal dialysate. In this way, it can be replaced 3-4 times a day, and the toxins and excess water in the body can be continuously discharged. After education and training, patients and their families have mastered the operation of peritoneal dialysis, and they can carry out peritoneal dialysis at home by themselves. If you use the automatic peritoneal dialysis machine, you can perform dialysis in your sleep every night, and you can work and study normally during the day. Advantages of peritoneal dialysis: (1) It is better to protect residual renal function than hemodialysis: peritoneal dialysis is the treatment scheme closest to physiological state, and there is no sudden change in hemodynamics, body fluid volume and biochemistry during peritoneal dialysis, thus reducing dialysis complications caused by unstable internal environment, such as cardiovascular diseases, hypertension, hypotension and arrhythmia. It will not cause renal ischemia during the treatment, which is beneficial to protect residual renal function. ⑵ Wide scope of application: Peritoneal dialysis has good cardiovascular stability and is the first choice for patients with serious cardiovascular diseases, cerebrovascular diseases, diabetes and the elderly; Abdominal dialysis has less dietary restrictions, better nutritional status of patients, less impact on children's growth and development, and avoids the pain of hemodialysis puncture; Abdominal dialysis does not need arteriovenous fistula, which avoids the occlusion of arteriovenous fistula caused by peripheral vascular diseases in diabetic patients. ⑶ The dialysis efficiency is high: the medium molecular toxin, β2 microglobulin and phosphorus are well removed. Therefore, peritoneal dialysis can improve the symptoms of uremia and improve anemia and neuropathy better than hemodialysis. ⑷ There is less chance of viral hepatitis B and C infection. 5] The degree of dialysis osteopathy in long-term dialysis is also better than that in hemodialysis. [6] Dialysis can be carried out at home, without going to the hospital, without affecting work, study and travel, with low treatment cost and high quality of life. Disadvantages of peritoneal dialysis: Peritoneal dialysis requires the insertion of peritoneal dialysis tube in abdominal cavity, and there are frequent operations such as changing peritoneal dialysis fluid during dialysis. If patients or their families do not strictly master aseptic operation, they are prone to infection and lead to peritonitis. However, with the improvement of peritoneal dialysis equipment, the strengthening of education and training for patients by peritoneal dialysis specialists and nurses, and the improvement of living and living sanitary conditions, the incidence of peritoneal dialysis infection has been greatly reduced. Peritoneal dialysis has been used to maintain the life of uremia patients for more than 30 years. At present, in Hong Kong and some European countries, 80% of uremia patients live, work and study under peritoneal dialysis treatment. However, both hemodialysis and peritoneal dialysis can only replace the kidney's function of removing metabolic wastes and maintaining the balance of water, electrolyte and acid-base, but can't replace another important function of the kidney, namely, the endocrine function, such as the production of EPO and active vitamin D3. Therefore, patients with maintenance hemodialysis or peritoneal dialysis still need to be treated with EPO, calcitriol and other drugs according to their condition. It is not what some patients think that "you don't have to take medicine when you do dialysis." Kidney transplantation is the most reasonable and effective treatment for uremia patients, but due to the lack of donors, kidney transplantation can not play its due therapeutic role. At present, there are only more than 5,000 kidney transplant recipients in China every year, and only one out of every 150 waiting patients may get a kidney transplant, and the shortage of donors has become a bottleneck restricting organ transplantation. Therefore, most uremic patients need long-term maintenance hemodialysis or peritoneal dialysis treatment. According to institutional statistics, there are about 100000 dialysis patients in China, with hemodialysis patients accounting for about 90% and peritoneal dialysis patients accounting for only 10%.