chronic and acute renal failure

chronic and acute renal failure

Classification of Diseases, Division of Nephrology description of chronic disease
Chronic renal failure renal failure, referred to as chronic renal failure, due to reduced renal units were destroyed, resulting in renal excretion of metabolic regulation and endocrine function caused serious damage to water and electrolytes, acid-base balance disorders appear a series of symptoms, signs and concurrent disease. Reasons for children with chronic renal failure and renal failure when 1st detected in children is closely related to the age. 5 years of age with chronic renal failure is often the result of anatomical abnormalities, such as renal hypoplasia, renal dysplasia, urinary tract obstruction, and other congenital malformations; 5 years later after the nature of chronic renal failure were glomerulonephritis with glomerular diseases such as small , hemolytic uremic syndrome or hereditary diseases such as Alport syndrome, renal cystic lesions based. Variety of chronic kidney disease, with disease progression, renal unit destruction, as well as the functional residual renal unit can not adequately discharge of metabolic wastes and maintain a constant internal environment, thereby dysfunction and urinary tract disorders in the environment, including waste and toxic metabolic the retention of water, electrolyte and acid-base balance disorders, and a series of clinical symptoms associated with the pathological process, known as the CRF (chronic renal failure.) Incidence of seve

re chronic renal failure stage
Treatment of chronic renal failure, said uremia, not a separate disease, is caused by a variety of causes progressive deterioration of kidney damage and, when developed to the end stage of renal function was similar to normal about 10% occurs when a series of comprehensive symptoms. Since renal impairment is a long process of development, different stages have different extent and characteristics, the general level of renal function should be split into several issues. Compensatory renal function impairment of renal function has not reached the total number of units of 1 / 2, does not produce elevated blood urea nitrogen and creatinine, metabolic balance, there are no symptoms (in the blood (Scr) creatinine in the 133-177 mol / L (2mg / dl)). Renal insufficiency of renal function fell below 50%, serum creatinine (Scr) level rose to 177 mol / L (2mg/dl) above, blood urea nitrogen (BuN) le 7.0mmol / L (20mg/dl) patients have fatigue, loss of appetite, nocturnal enuresis, mild anemia and other symptoms. Renal failure, when the students of
Chronic renal failure creatinine clearance rate (Ccr) decreased to 25ml/min the following, BuN higher than 17.9 - 21.4mmol / L (50 ¯ 60mg/dl), Scr rose 442 mol / L (5mg/dl) above, patients had anemia, serum phosphate levels rise, blood calcium decreased, metabolic acidosis, fluid and electrolyte disorders. Ccr 10ml/min end-stage uremia in the following, Scr rose 707 mol / L or more, significant acidosis, the symptoms appear, and even coma. Watch for symptoms and signs of nausea, vomiting, diarrhea, lower limb must move often unbearable burning, itching, pain, convulsions and other signs of bleeding. Physical examination: Note respiratory rate, depth, whether the ammonia odor, pay attention to the state of consciousness, the degree of anemia, with or without muscle twitching, dehydration, edema, oral mucosa ulcers, pericardial friction rub, pay attention to whether the blood pressure and heart failure symptoms. Note whether the cause of acute disease, chronic nephritis, acute and chronic pyelonephritis, renal arteriosclerosis, renal tuberculosis, urinary tract obstruction, systemic lupus erythematosus, diabetes, gout, multiple myeloma and polycystic kidney disease, and long-term taking anti-inflammatory agents and a history of exposure to heavy metals. Note: 1. Should strive to clear the cause of chronic renal failure, kidney damage is at least clear the main glomerular damage, or to renal interstitial tubular lesions based, or to highlight the renal vascular lesions in order based on clinical characteristics, treatment focused. 2. Should be identified with chronic renal failure to promote the sexual development of renal function reversible factors, such as infection, metabolic acidosis, dehydration, heart failure, low blood pressure too fast, too low and so on. 3. Should be looking for increased attention to chronic renal failure of renal function decline of certain factors, such as hypertension, hyperlipidemia, hypercoagulable state, high-protein diet intake, proteinuria and so on. Glomerular disease mechanisms for the mechanism of damage: the basis of clinical observation, progression of uremic patients have their laws, and is a progressive deterioration of the process. If the above stages, when patients enter the stage of renal insufficiency, serum creatinine of 442umol / L (5mg/dl) level, the development of end-stage uremia, the average time was 10.8 months. The main theory of the mechanism are the following: 1, glomerular filtration theory that excessive progression of the important cause of uremia is due to excessive residual renal glomerular filtration units, resulting in glomerular sclerosis in succession. It is known that reduced renal parenchyma, such as partial nephrectomy, the remnant of a single nephron glomerular filtration rate increased glomerular input and output to reduce the resistance of small arteries, thus increasing the blood flow rate of a single glomerulus. Meanwhile, the input resistance to reduce the level of small arteries is greater than the output of small arteries, prompting the glomerular capillary pressure gradient increases across. These constitute the glomerular filtration rate of residual renal units (GFR) increased or decreased the extent and degree of renal related, such as the side of the nephrectomy, the average increase of 40 ¯ 50%; while 80% of renal parenchyma after resection, the residual kidney GFR, twice the increase will be larger than normal. According to the experiment, SNGFR = K1 * PnF K1 = ultrafiltration coefficient, PnF = average net ultrafiltration pressure. As can be seen from the above equation, the size of these two values to determine the size of SNGFR. K1 even a significant reduction in the renal unit, the residual renal unit ball K1 little change in the role of an increase in SNGFR, PnF play a decisive role. PnF size in turn depends on the following three factors: capillary hydrostatic pressure ( P); plasma protein concentration (CA); glomerular plasma flow (QA). One CA more constant, PnF decided P and QA. When nephron loss, residual renal unit "compensatory" or "adaptation", P and QA are increased with each other, thus SNGFR increased. This excessive filtration, although a compensatory role, but in turn, cause damage to residual renal glomerular units. Nephrectomy as 85% of the animals, 3 months shows residual glomerular hypertrophy, epithelial cell exfoliation, mesangial expansion and capillary area of the cavity loss of elasticity, leading to focal segmental glomerulosclerosis. On the other hand, capillary pressure and blood flow increased, prompting macrophages outside the movement and access to the capillary membrane area, these have all contributed to hardening the ball. These changes have led to further reduce the renal unit, resulting in residual glomerular filtration rate increases, the emergence of new diseases and new hardened, creating a vicious cycle, the condition worse. 2, an imbalance of righting a wrong theory of uremia, some caused by toxic effects of humoral factors, the concentration increased gradually in the body is not entirely due to a decrease in renal clearance, but a balance to adapt to the body; but in the process of adaptation, has emerged new imbalances, again and again, causing the body to damage. If the blood thyroid hormone (PTH), for example, when the GFR decreased uremia, urinary phosphorus excretion decreased, there hyperphosphatemia stimulate parathyroid secretion of PTH, acting on the renal tubules, increased urinary phosphate excretion, the lower phosphorus return to normal levels. However, due to the loss of kidney function are more, PTH levels in the extracellular solution rising, is still difficult to correct hyperphosphatemia, and increased product of serum calcium, intracellular calcium increase, resulting in extensive multi-system in the body of calcium and phosphorus deposition, which also includes the kidneys themselves. As a further decline in GFR, then there hyperphosphataemia. This cycle results so that the constant increase in plasma PTH levels, renal unit for further damage. Uremia, serum and urine increased natriuretic hormone levels, indicating reduced renal clearance rate of its increase is not reason, may generate an increase in the body is the main factor. When the uremia, GFR decline, a decrease in sodium excretion tendency to compensatory hypertrophy of residual renal units, urea accumulation induced osmotic diuresis has not regulate sodium balance, this time increased natriuretic hormone, the fractional excretion of sodium increased in recent tubular sodium reabsorption decreased. However, natriuretic peptide on the Na - K-ATP inhibited the enzyme activity, so the increase can also enable many cells to sodium and other substances that barriers to active transport, the formation of some new damage. PTH natriuretic peptide itself is not "toxic" substances, but in this case, the rising levels in the body, forming a new "poison." Excessive filtration theory, that the uremia, the glomerular damage were the main reason for the prevention and treatment of uremia provides a theoretical basis. Imbalance correction theory, highlighting the formation of uremia, the body imbalance, resulting in some of the excess material, the formation of uremic symptoms, treatment of these imbalances can reduce symptoms, such as partial resection of parathyroid glands, or trying to control the following recurrent hyperparathyroidism, uremia to alleviate the symptoms is important. 3, "toxin" theory currently known uremic patients is elevated over 200 substances, toxic effects may be, approximately 20 species. These substances have the following characteristics: the publication of chemical substances can be identified and quantitatively. content than normal concentration in vivo. high concentration and specific symptoms of uremia. experiments confirmed that the concentration of the substance concentration in body fluids of patients with uremia similar, similar toxic effects. Progressive deterioration of chronic renal failure mechanism and the mechanism is not yet completely understood. Deterioration of renal function based on the disease activity and no doubt related. But despite the underlying disease activity has stopped, such as the GFR has fallen to about 25% of normal, the kidney function will continue to decline constantly, until uremia, and its reduction through a common pathway. At present, most scholars believe that, when damaged to a certain number of renal units, the remaining "healthy deposit" of renal excretion of metabolic waste unit load increases, the need to maintain normal body. Thus compensatory high occurrence of glomerular capillary perfusion, high pressure and high-filtration (glomerular "three high"). The glomeruli of the "three high" can cause: glomerular epithelial cell foot process fusion, mesangial cells and matrix were significantly hyperplasia, glomerular hypertrophy, and subsequent hardening; glomerular endothelial cell injury, induced platelet aggregation , leading to micro-thrombosis, damage to the promotion of glomerular sclerosis; increased glomerular permeability, proteinuria increased to tubulointerstitial injury. The process continues, creating a vicious cycle in which further deterioration of renal function continuously. This is all the development of chronic kidney disease, a common way to uremia. Angiotensin (angiotensin, A ) in the progressive deterioration of renal failure plays an important role. In the glomeruli of "three high", the renin-angiotensin axis activity increased, while the A is a powerful vasoconstrictor substances, whether caused by the systemic circulation A increased blood pressure, kidney or local A increased, can be lead to increased glomerular capillary pressure, causing glomerular hypertrophy, and then rise to glomerular sclerosis. In addition, A has nothing to do with the blood pressure to rise to the following functions: involved in extracellular matrix (ECM) synthesis, and excessive accumulation of ECM occurs glomerulosclerosis; A increased transforming growth factor 1 (TGF- 1), platelet-derived growth factor (PDCF), interleukin -6 (IL-6), platelet activating factor (PAF), thromboxane A2 (TXA2) and other growth factors, inflammatory cytokines and fibrosis factor expression, and TGF- 1 is ECM synthesis and fibrosis of the kidney decisive media, will lead to occurrence of glomerulosclerosis. AII the glomerular capillary blood pressure, can cause increased glomerular permeability, too much protein from the glomerular filtrate, proximal tubule cells by endocytosis after its absorption, can cause renal damage, between interstitial inflammation and fibrosis, resulting in the loss of nephron function. Research shows that in the culture of the proximal tubule cells to absorb albumin, can growth factors, inflammatory cytokines and fibrosis factor expression. Present the that the deterioration of renal proteinuria is an important factor. The rate of deterioration in recent years that a genetic kidney failure, such as angiotensin converting enzyme gene and the rate of renal dysfunction has an important relationship. TCM chronic renal failure patients identified by the disease nausea, vomiting, poor appetite, mouth with urine smell, urine night more or oliguria, edema, backache, limbs lack, Shenpi, headache, irritability, Nvxue, minimalist looking, skin A mistake as the main clinical manifestations, can be attributed to medicine "off grid", "female drug", "Consumption" and other ranges. Pathogenesis of critical right for the San Jiao, poisoning caused by damp cholestasis retention; disease located in the kidney and spto internal organs. Most of the patients in critical condition, the prognosis is poor, expressed as yin and yang imbalance, deficiency and excess mixed the cards. Early clinical manifestations, often only the symptoms of disease, performance-based. 1. Residual renal unit can not be adjusted to adapt to the body requirements, renal failure symptoms occur 2. Renal disease is very complex and can affect various body organs, constitute the performance of 3 uremia. The majority of dialysis can improve the symptoms of uremia, but some symptoms sustainable or even add to symptoms: 1, gastrointestinal tract: the first, the most common symptoms are: a. anorexia (loss of appetite first) b. nausea, vomiting, abdominal distension c. tongue, mouth ulcers ammonia smell mouth d. upper gastrointestinal bleeding taste e. 2, blood system: a. Anemia: Patients must have symptoms of uremia. The degree of anemia and uremia (kidney function) degree parallel, C EPO Erythropoietin (EPO) to reduce the major causes b. bleeding tendency: can be expressed as the skin, mucous membrane bleeding, and increased destruction of platelets, prolonged bleeding time and other related may be caused by toxins, dialysis can quickly correct the abnormal white blood cells c.: reduced chemotaxis, phagocytosis and bactericidal ability of weakened, prone to infections, dialysis can improve the 3, the cardiovascular system: the most common cause of death was renal failure a. hypertension: most patients have varying degrees of volume-dependent hypertension renin dependent + can cause arteriosclerosis, left ventricular hypertrophy, heart failure b. heart failure: the performance of cardiomyopathy often appear, Shuinazhuliu; hypertension; uremic cardiomyopathy and other disorders caused by c. pericarditis: urea or disease due to inadequate dialysis, mostly bloody, usually late manifestations d. atherosclerosis: progress rapidly, even more apparent in hemodialysis, coronary artery, cerebral artery, the body may occur around the artery is mainly due to hyperlipidemia and hypertension 4, nerve, muscle system performance: a. Early: fatigue, insomnia, inability to concentrate, etc. b. late: peripheral neuropathy, sensory motor nerve was significantly higher than c. dialysis disequilibrium syndrome: rapid decrease of urea nitrogen, osmotic balance inside and outside cells, causing increased intracranial pressure and cerebral edema, the performance of nausea, vomiting, headache, severe cases, convulsions. 5, renal osteodystrophy: when the bone changes is the general term uremia can cause spontaneous fractures a. b. symptoms are rare, such as bone pain, inconvenience walking 6, the performance of the respiratory system: a. Deep breathing during acidosis and long b. uremic bronchitis, pneumonia (butterfly wings), pleurisy, etc. 7, skin symptoms: skin itching, urea frost deposition, uremic face, dialysis does not improve 8, endocrine disorders: a. hormone produced by the decline in renal b. degradation of the hormone in the kidney can be increased by 9 and easy with severe infections: infection, fever was 10 not normal, metabolic disorders and others: a. Hypothermia: body temperature less than normal about 1oC (estimated fever should be considered) , basal metabolic rate of glucose metabolism often fall b.: General patients: impaired glucose tolerance; diabetic patients: insulin dosage should be reduced (to reduce degradation) c. lipid metabolism: TC normal d. hyperuricemia: GFR 13.5mmol / l (30 volume%), and there is acidosis symptoms can be used 200ml of 5% sodium bicarbonate infusion, or 11.2%, intravenous infusion of sodium lactate lOOml diluted to 600ml. Such as edema, high blood pressure who used ammonia butyrate 3.64% glycerol (THAM) 200ml intravenous infusion. 7. Thoughts
Infected with chronic renal failure factors should actively control the infection with antibiotics. 8. To try adsorbents, such as oxidized starch, 30 ~ 50g / d, split Oral; medicinal charcoal 40g / d, taken orally several times, the role of lowering blood urea nitrogen. 9. Oliguria, edema were available furosemide (furosemide) 40 ~ 100mg intravenous, 1 / 6 ~ 8h, or of the urinary amines lmg, 1 / 6 ~ 8h. But disable potassium type diuretics should not increase the hyperkalemia. 10. Was use of antihypertensive drugs in hypertensive patients to use A-CEI-based, such as captopril (25 ~ 100mg, 3 / d), enalapril (5 ~ 10mg, 1 / d), benzene Enalapril (5 ~ 20mg, 1 / d), drug use principles with acute nephritis, blood pressure should not be too fast, too, in order to maintain diastolic blood pressure in 13.3kPa (100mmHg) is appropriate, should not reduce urine output, and observe whether the incidence of hyperkalemia. With heart failure may use digitalis preparations, but the dose should be reduced more commonly used 1 / 2 to 1 / 3. Severe anemia, erythropoietin treatment available, subcutaneous injection of 2 to 3 times / week, 1500 ~ 3000U / times. Appropriate blood transfusion when bleeding. Nausea, vomiting, who was available metoclopramide (metoclopramide), domperidone (Motilium) or chlorpromazine (Dongmian Ling). 11. Dialysis therapy: a conditional should be promptly implemented. 12. Allogeneic kidney transplantation: indications and have received a transplant conditions and subjected to those donors who can select the appropriate immunization. Health Tips Food: 1, the focus of diet therapy is to limit the intake of protein to reduce the quality of nitrogen retention. But to pay attention to ensure adequate calories and sufficient essential amino acids. Specific to each patient''s protein intake should be in accordance with its clearance rate in the study muscle flexibility. 2, adhere to high-quality low-protein diet, low phosphorus, low-salt, high-calorie; to avoid aggravating factors, appropriate cold temperature, cold shelter from the wind; avoid exogenous, infection, diet and restrained. Prevention: 1, to avoid overwork and a strong mental stimulation; 2, prevention of infection, removal of foci in order to reduce the incentive condition deteriorated 3, alcoholic drinks and tobacco addiction should quit; 4, edema, hypertension, significant proteinuria and take a action is increased symptoms who were advised to stay in bed. Note: 1, and oral care, reduce the stimulation, the prevention of oral ulcers, affect consumption. 2, the patient has a headache, insomnia, irritability, indoor light to dark, to facilitate the patient is at rest, if necessary, with a sedative, can serve stability and so on. 3, high blood pressure, blood pressure should be measured regularly, the condition of patients with antihypertensive drugs, and should adhere to regular use. 4, there is bleeding, the use of hemostatic agents under the doctor asked. 5, to protect skin and prevent occurrence of pressure sores and abrasions. 6, a serious condition, promptly sent to the hospital for hemodialysis or peritoneal dialysis to do. Information uremic toxins: is generally divided into small molecules (molecular weight <500dal), the molecule (molecular weight of 500 ¯ 5000dal) and macromolecules ( 5000dal) categories. Toxic molecules, one of the most cited are from the attention of urea, guanidine. Macromolecules a urea: uremia, the largest concentration in body fluids of a metabolite. Very high serum concentrations, can cause headaches, fatigue, nausea, vomiting, drowsiness, bleeding tendency and so on. The toxicity of urea on the duration of its existence, its metabolites can cyanates of proteins carbamoyl, an important relationship with the symptoms of uremia. guanidine: guanidine certain amino acids and creatinine metabolism, the animals injected large amounts of methyl guanidine, there may be a series of similar symptoms and uremia. GUANIDINE positively charged, easy and cells with negatively charged phospholipids in the cell accumulation, the formation of cytotoxic. The formation of methyl guanidine and creatinine levels parallel. When the urine volume of less than 400ml / d, the plasma and urine methyl methyl guanidine guanidine are rising. Guanidine Guanidine succinate toxic than methyl weak, normal urinary excretion of 10mg per day about 5 times increase when uremia. The role of guanidine succinate are: inhibit platelet adhesion and aggregation, inhibit platelet factor . promote their hemolysis. inhibition of lymphocyte function. disorder caused by brain activity. amines: include fatty amine spin, spin aromatic amines and polyamines. High concentrations of fatty amine rotation (1 - methylamine, 2 - methylamine, 3 - methylamine, etc.) can cause myoclonus, tremor, and hemolysis-like flapping wing can also inhibit the activity of some enzymes. Aromatic spin amines (amphetamine, tyramine) on the chlorination process of brain tissue, succinic acid oxidation and dopa carboxylase activity of inhibit. Polyamines, including spermine, fine, putrescine and cadaverine. High concentrations of polyamines can cause anorexia, nausea, vomiting, and proteinuria, and promote dissolution of red blood cells, inhibit the generation of erythropoietin, inhibition of Na-ATP enzyme and Mg2-ATP activity, but also increase the permeability of the microcirculation promote uremic lung, acute pulmonary edema, ascites, and the generation of cerebral edema. Second, application of molecular substances in the chromatography technique confirmed that the plasma in uremic patients can be found 8 ¯ 9 a clear peak, severe patients, the peak No. 7 is particularly evident. Peritoneal clearance of urea is lower than the artificial dialysis membrane of about 4 ¯ 6 times, but the peritoneal removal of high molecular substances in the artificial membrane. Although the decline in peritoneal dialysis patients with slow blood urea nitrogen, but the lifting of the symptoms of the nervous system better than hemodialysis excellent support in of molecular substances cause toxicity. Toxic substances in the molecule may include: high concentration of normal metabolites. structure of normal, elevated concentrations of the hormone. cell peptide produced by metabolic disorders. cells or bacterial lysate. Depth in the high molecular substances can cause peripheral neuropathy, uremic encephalopathy, inhibiting erythropoietin, insulin inhibition, inhibition of antibody production, platelet dysfunction, immune dysfunction, sexual dysfunction, and exocrine gland atrophy. The role of the three PTH uremic patients with secondary hyperparathyroidism often and plasma parathyroid hormone (PTH) levels. Cause of its formation may be due to increased phosphate; bone calcification on the role of PTH resistance; caused by changes in vitamin D metabolism. PTH levels can cause multiple organ damage, PTH can cause increased intracellular calcium concentration, the ratio of change in intracellular calcium affect cell membrane permeability, to promote soft tissue calcification, increased protein metabolism in nitrogen accumulation in the blood. PTH of the "toxic" role performance are the following: EEG changes due to elevated blood PTH. Delayed motor nerve conduction velocity. Brain Ca2 content increased. PTH levels is one important reason for the formation of anemia. The main way to PTH can inhibit the red blood cell production, can reduce the survival of red blood cells can cause bone calcium and bone marrow fibrosis free. PTH effects on the heart. The heart is the important target organs of PTH, which can affect heart function and cardiac cell metabolism. Renal failure drug Principles 1. A term used by early mild, and pay attention to controlling the amount of liquid into, vitamin supplements and energy to maintain electrolyte and acid-base balance; 2. Myasthenia should be timely, early for dialysis treatment, dialysis, peritoneal dialysis can choose maximize the protection of residual renal function; attention complications such as hypertension, anemia, proteinuria,,,, so as to correct reversible factors on kidney damage; needed dialysis every day, and to the transfusion of blood and human albumin; 3. co-infection depending on the circumstances when the drug selected C item; 4. with hypertension, the choice of A or C items of drug items; 5. with heart failure, it can be cedilanid other cardiac medications; 6. hemorrhage A term used when the drug or the C key. Misdiagnosis of chronic kidney failure Wu suffering "gastritis" has been 5 years, after the Spring Festival, he suddenly appears again bleeding, no significant improvement after treatment of the disease is still intermittent bleeding. Zhengzhou City Hospitals for him to do a system check and found that Mr. Wu even with chronic renal failure. Chronic renal failure is a systemic multi-system against serious illness, sometimes, because the symptoms of a system was especially prominent, easily misdiagnosed. Suffering from kidney disease, digestive system will be abnormal why it? This is because when renal damage, decreased urinary excretion of toxins, the blood will increase the toxin, the toxin also increased discharge from the digestive tract, gastrointestinal mucosa by LPS, causing the stomach, duodenum mucosa superficial inflammation, ulcers and even lead to upper gastrointestinal bleeding. Clinically, chronic renal failure patients often see long term, gastroenterology, and endoscopy are indeed pathological, not knowing that this is one of the complications of chronic renal failure. In the early chronic renal failure, most patients have no symptoms, blood disorders were not evident, only showed hypertension, proteinuria and serum uric acid levels increased slightly. Wu Xianming reminded, want to keep at these suspicious circumstances, in order to avoid misdiagnosis. Early detection of renal failure is the only way to do kidney function tests, for the reaction of the digestive tract caused by kidney disease, the most important should be treated renal failure. Gastrointestinal symptoms that had appeared to be closely observed, suggesting that patients eat digestible, non-stimulating food. For loss of appetite, nausea, vomiting, patients should stay in bed. Children with chronic renal failure treatment in children with chronic renal failure which required monitoring of treatment of children with clinical (physical examination and blood pressure) and laboratory tests including hemoglobin, electrolytes (hyponatremia, hyperkalemia, acidosis), blood Determination of urea nitrogen and creatinine, calcium and phosphorus levels and alkaline phosphatase activity. Regularly check the level of parathyroid endocrine and bone X-ray for early detection of bone dystrophy. Chest radiography and echocardiography may help to understand cardiac function. Nutritional status can regularly check serum albumin, zinc, conversion of iron, folic acid and iron levels to monitor. 1. Chronic renal failure diet to normal when the glomerular filtration in children less than 50% when the growth rate in children decreased, mainly due to a lack of calories. Although not when the renal dysfunction, what is the appropriate calorie intake, but as far as possible equal to or higher than the caloric intake of children age group. Unlimited increase in available carbohydrate intake of dietary calories, such as sugar, jam, honey, glucose polymers and fatty oils such as medium chain triglycerides, subject to the patient can tolerate. When urea nitrogen higher than 30mmol / L (80mg/dl) when the patient can be nausea, vomiting and anorexia, which can be due to limited protein intake and ease. Children still in renal failure due to a certain amount of protein for growth, it is a protein 1.5g / (kg · d), and containing large amounts of essential amino acids should be given to high-quality proteins (egg and lean meat), such as eggs, milk , followed by the meat, fish, chicken and poultry. Milk phosphorus is too high, not appropriate to use, have to use glucose, a type of food to supplement the peanut oil heat. Because loss of inadequate intake or dialysis, pediatric renal insufficiency, there may be water-soluble vitamin deficiency should be routine supplementation. If trace elements are iron, zinc deficiency also have to supply fat-soluble vitamins such as A, E, K is not necessary to add. 2. The treatment of water and electrolytes in children with renal insufficiency, rarely to be limits on the amount due and the brain "thirst centers" to adjust, unless the development to be used with end-stage renal failure dialysis. Most children with renal insufficiency with the appropriate diet to maintain normal sodium balance. Some patients because of anatomical abnormalities of renal insufficiency, by the loss of a large number of urinary sodium, dietary supplements are required by the sodium; the other hand patients with hypertension, edema, or congestive heart failure should restrict sodium, sometimes combined with furosemide, 1 4mg / (kg · 24h). Further deterioration of renal function, such as when required to do dialysis. Hyperkalemia may first try diet plus oral intake of potassium or lower potassium alkaline material resin (sodium polystyrene sulfonate, Kayexalate) treatment. Renal insufficiency in children almost all of acidosis, and generally do not need treatment unless serum bicarbonate less than 20mmol / L, shall be corrected with sodium bicarbonate. 3. Renal osteodystrophy when hyperphosphatemia, hypocalcemia, increased parathyroid endocrine levels and serum alkaline phosphatase activity increased, often with renal osteodystrophy. Generally when the glomerular filtration rate of 30% or less to normal, the serum phosphorus levels rise. Decreased serum calcium, secondary hyperparathyroidism. Hyperphosphatemia and low available phosphorus in the diet, calcium or bicarbonate can also be used to promote oral antacid phosphorus from the intestinal tract. Aluminum toxicity in children to pay attention to the problem, regular monitoring of serum aluminum levels. Severe renal insufficiency and vitamin when D (Vit.D) lack, Vit.D for continuous low blood calcium, X-ray showed rickets and serum alkaline phosphatase activity increased time. 4. Anemic patients with hemoglobin stability in the majority of 60 ~ 90g / L (6 ~ 9g/dl), without blood transfusion, such as hemoglobin less than 60g / L were carefully enter the red blood cell 10ml/kg (a small amount of blood circulation to reduce the risk of overload.) 5. High blood pressure in hypertensive emergencies with sublingual nifedipine can be injected or antihypertensive hydralazine is diazoxide (5mg/kg, maximum dose 300mg, injected within 10 seconds.) Severe hypertension with blood circulatory overload can be given furosemide (2 ~ 4mg/kg, speed 4mg/min). Renal insufficiency, should be careful application of sodium nitroprusside, may have because of the accumulation of thiocyanate. In short should seek early diagnosis, remove the cause, if found too late, though removal of the cause, of renal tissue damage has been difficult to recover. If the patient because of urinary tract obstruction, surgery should be done accordingly, but often in children with renal insufficiency can not tolerate too much surgery can do first kidney gastrostomy or suprapubic bladder fistulization to facilitate drainage. If continuous or intermittent pyuria, infection control should be active, and track re. For end-stage renal disease or renal failure is difficult to restore the patient, the blood in recent years, application of chronic dialysis (artificial kidney, blood, also known as long-term intermittent dialysis), many patients can survive or return to normal life. The current long-term regular dialysis, usually 2 to 3 times a week dialysis, can sleep at night dialysis. Blood in patients undergoing chronic dialysis treatment in children, the development of secondary sexual characteristics, such as weight gain had no significant effect on height only slightly affected. In recent years, the implementation of foreign chronic blood dialysis patients from the hospital transferred to the family, has been long on dialysis in children 4 to 5 years. Peritoneal dialysis for chronic renal failure has been the main long-term fixed within the catheter in the abdominal cavity, the daily dialysis on time, in the family can be carried out in accordance with doctor''s orders. Treatment of children with end-stage renal failure is the ultimate goal of kidney transplantation. 5 years of age in a foreign country the success rate of kidney transplantation in children and adults the same as before renal transplantation (a continuation of life in order to make children to wait for suitable donor kidney), or kidney transplant rejection phenomenon occurs after all depend on effective chronic blood dialysis. A chronic renal failure and the diseases easily confused with 1. Prerenal acute renal failure due to renal factors make the effective circulating blood volume before the reduction in renal blood flow caused by hypoperfusion caused by renal damage. Reduced glomerular filtration rate, renal tubular urea nitrogen, water, and the relative increase in sodium reabsorption, blood urea nitrogen were increased, decreased urine output, urine specific gravity increased. Prerenal acute renal failure in patients with glomerular and tubular structures remained intact, when kidney perfusion returned to normal, glomerular filtration rate recovered. But serious or persistent renal hypoperfusion can make the development of prerenal acute renal failure to acute tubular necrosis. (1) Effective hypovolemia: bleeding: trauma, surgery, postpartum, digestive tract. digestive fluid loss: vomiting, diarrhea, gastrointestinal decompression, and so on. kidney loss: diuretics, diabetes, acidosis. loss of skin and mucous membrane burns, high fever and so on. The third compartment is missing: crush syndrome, pancreatitis, hyperlipidemia, etc. Low albumin. (2) reduced cardiac output include: congestive heart failure, cardiogenic shock, cardiac tamponade, severe arrhythmia. (3) systemic vascular expansion: sepsis, liver failure, allergic reactions, drugs (antihypertensive drugs, anesthetics). (4) renal vasoconstriction: norepinephrine and other drugs, application, sepsis, liver failure and so on. (5) self-regulation of renal vascular drugs: angiotensin converting enzyme inhibitors, non-steroidal anti-inflammatory drugs. 2. Kidney after acute renal failure (1), ureteral obstruction: cavity obstruction: crystals (uric acid, etc.), stones, blood clots and so on. cavity obstruction: retroperitoneal fibrosis, tumor, hematoma. (2), bladder neck obstruction: prostatic hypertrophy, bladder neck fibrosis, neuron bladder and prostate cancer. (3) urethral obstruction narrow. 3. Renal acute renal failure (1) renal disease: the most common acute tubular necrosis. Cause of sub-renal ischemia and renal toxicity. renal ischemia: prerenal causes of acute renal failure is not lifted in time. nephrotoxicity: nephrotoxic common substances, such as drugs, contrast agents, heavy metals, biological toxins, organic solvents, myoglobinuria, hemoglobinuria, light chain protein and hypercalcemia. (2) glomerular diseases: such as rapidly progressive glomerulonephritis, lupus nephritis. (3) acute interstitial nephritis: acute (allergic) drug-induced interstitial nephritis, sepsis, severe infection. (4) renal microvascular disease: primary or secondary necrotizing vasculitis, malignant hypertension, renal damage. (5) acute renal macrovascular disease: kidney bilateral or unilateral renal artery / renal vein thrombosis or embolism of cholesterol crystals; false floor bleeding aneurysm, renal artery rupture. (6) some of the chronic kidney disease: deterioration in the factors promoting the role of chronic renal failure, leading to acute exacerbation of chronic renal failure, acute renal failure in clinical manifestations. 2

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