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Sunday, February 19, 2012

Renal Failure Introduction

Renal failure-About Renal failure:

Renal failure - Introduction
Renal failure can be divided into acute and chronic, acute renal failure progression quickly and is usually due to insufficient supply of renal blood flow (such as trauma or burns), kidney obstruction due to some factors that cause functional impairment or by poison damage caused by acute renal failure. Chronic renal failure mainly due to the long-term kidney disease, kidney function gradually decreased with time and disease caused by the occurrence of renal failure. Hope of recovery. Only two ways to treat for chronic renal failure, dialysis treatment or kidney transplant.

Renal failure etiology:Patients with renal failure caused by a variety of causes of acute tubular necrosis, can be summarized into two broad categories:Nephrotoxic substances toxic to the kidneys, such as sulfa drugs, carbon tetrachloride, mercury agent, bismuth the dichloro sulfa (dichlorphenamide,); polymyxin antibiotics, vancomycin, the card that mold factors, gentamicin, Vanguard ADM I, Vanguard ADM II, neomycin, amphotericin B, and iodinated contrast media, methoxy halothane anesthetics; biological toxins such as snake venom, bee venom, fish, mushroom, cantharidin (cantharidin), can under certain conditions, to cause acute tubular necrosis.Severe renal ischemia and renal ischemia, such as heavy degree of trauma, extensive burns, major surgery, massive blood loss, postpartum hemorrhage, severe infection, sepsis, dehydration and electrolyte imbalance, especially combined with shock who are easily lead to acute tubular necrosis.In addition, intravascular hemolysis (blackwater fever, primaquine-induced hemolysis, favism, blood type incompatible blood transfusion, the oxidation of arsenic poisoning) released from hemoglobin, as well as muscle mass trauma (eg, crush injuries, muscle inflammation) myoglobin excretion through the kidneys, renal tubular damage caused by acute tubular necrosis.Specific pathogenesis of acute tubular necrosis of the myoglobin is not yet fully understood. It occurred with the following:(1) glomerular filtration rate is extremely lower (often following in 5ml/min, the majority only 1-2ml/min) generated mechanism may be due to the aforementioned variety of causes tubular ischemia or poisoning, the occurrence of renal tubular epithelial cell injury , so that the proximal tubule sodium reabsorption decreased, resulting in the original urine sodium, the amount of water increased. When its flowing through the macula densa of the distal convoluted tubule to stimulate the juxtaglomerular (juxtaglomerularapparatus) the release of renin, angiotensin Ⅱ activity increased in the kidney, caused by the contraction of the glomerular arterioles spasm, leading to glomerular cortex, the outer layer of the glomerular blood flow decreased, the extreme reduction in filtration rate. Also may be due to renal ischemia, renal afferent arterial perfusion of blood to reduce the direct stimulation of juxtaglomerular cells release renin leaving the angiotensin II increased, resulting in afferent arteriolar constriction, glomerular filtration rate and the secretion of aldosterone to promote sodium and water retention. Some scholars believe that the glomerular filtration rate due to capillary endothelial damage, swelling, causing the permeability of the filtration membrane, reduce.② tubular cavity blocked by necrosis after injury, shedding of renal tubular epithelial cells and inflammatory exudate, red blood (muscle) protein to form clumps and tube, blocking the lumen, so that the original urine dirty blocked, and thus oliguria; lumen on the other hand the plot of urine swelling, will increase intrarenal pressure, glomerular filtration rate to decline further.(3) tubular wall rupture, the spillover of the original urine. Tubular injured after wall rupture, the original urine tube to overflow pipe outside, thus oliguria; at the same time lead to renal interstitial edema, increased intrarenal pressure, glomerular filtration rate.To ④ someone that a variety of reasons (shock, trauma, crush injuries, etc.) caused by renal ischemia-induced acute renal failure, mainly due to reperfusion after ischemic and early ischemic renal filtration to reduce or (oliguria or anuria) is to stop the kidney of a protection mechanism, mitigate reabsorption burden of renal tubular cells, reduce oxygen consumption, increased tolerance to hypoxia, renal ischemia improved (reperfusion). can produce large amounts of superoxide anion cause severe renal tissue damage, in short, acute renal failure with a characteristic syndrome consisting of a variety of physiological abnormalities, a variety of pathogenesis of various periods in the course of its different meanings.The oliguria urine of renal tubular epithelial freshmen, this time due to:The ① risk factors has been lifted, ischemic and toxic substances have been eliminated, blood circulation has been restored;② the nascent tubule cells still lack the ability to concentrate urine specific gravity was still lower than 1.015;③ azotemia and retention slip metabolites since the role of osmotic diuresis, the increased urine output, called polyuria phase.

Renal failure - pathogenesisPathogenesis of renal failure in patients with acute renal failureNaked eye to see increased kidney volume, soft, pale section of renal cortex, ischemia, medullary dark red. Microscopically, the renal tubular epithelial flattened, showed some cloudy swelling, degeneration, falling within the lumen tube and exudate. Nephrotoxicity caused by epithelial cell degeneration, necrosis concentrated in the proximal tubule, protect the integrity of the basement membrane; renal ischemia, epithelial cells showed focal necrosis, scattered tubular paragraphs, and its basement membrane is often broken, ulceration, renal interstitial visible small Park cell infiltration and edema in part died of acute tubular necrosis in patients with renal tubular morphology under the optical microscope did not change, so the tubular necrosis name, is not very appropriate, but these cases, electron microscopy, and sometimes still see the mitochondria of renal tubular epithelial cells to deformation, the endoplasmic reticulum disappears, the micro-cilia loss, some parts of the basement membrane micro-gap. Glomerular and renal artery is generally no change, only the occurrence of disseminated intravascular coagulation, will see in the glomerular capillary fibrin thrombus. Disease of the first 5-6 days, necrosis of tubular epithelial cells start a new life. If the basement membrane integrity, the nascent epithelial cells quickly cover in the basement membrane, tubular morphology returned to normal. Basement membrane is the destroyer of the epithelial cells can not regenerate, the defect is replaced by connective tissue.Renal failure - clinical manifestationsRenal failure, acute tubular necrosis (ATN) and renal acute renal failure is the most common type, usually according to their etiology into ischemic and renal toxicity. But clinically often multiple factors, such as occurs in critically ill comprehensive, including In addition to the toxic disease, renal hypoperfusion and renal toxicity of drugs and other factors.Typical of the clinical course can be divided into three phases:1, renal failure - the start ofThis period, patients often suffer some of the ATN, known etiology, such as hypotension, ischemia, sepsis and renal toxins. Renal parenchymal damage but has not yet occurred. At this stage of acute renal failure is preventable. But with the tubular epithelium was damaged, the GFR, a sudden drop in the performance of acute renal failure syndrome in the clinical became apparent, then enter the maintenance phase.2, renal failure - the maintenance periodAlso known as oliguria. Typical for 7-14 days, but can also be as short as a few days, as long as 4-6 weeks. Glomerular rate remained at a low level. Many patients, there may be oliguria (<40Oml / d). But some patients can not oliguria, urine output more than 400ml / d, referred to as non-oliguric acute renal failure, the disease mostly lighter, better prognosis. However, regardless of the amount of urine whether the reduction in renal dysfunction, can be a series of clinical uremia performance.Infection is another common and serious complications of acute renal failure. Acute renal failure at the same time or in the development of the disease process can also merge multiple organ failure, patient mortality can be as high as 70%.3, renal failure - recoveryRenal tubular cell regeneration, repair, restore tubular integrity. Glomerular filtration rate gradually returned to normal or near normal range. Oliguric patients began to appear diuretic, how much urine the performance of daily urine output up to 3000-5000ml or more. Usually lasts 1-3 weeks, then back to normal. Compared with the glomerular filtration rate, the recovery of the glomerular epithelial cell function (solute and water reabsorption) is relatively delayed, and often take several months after recovery. The small number of patients may be the ultimate legacy varying degrees of renal structural and functional defects.

Renal failure - renal failure in the family diet recipe(1) rhubarb, SJ, Guizhi 30 grams, add water to cook to the residue. Retention enema the day 1-2 doses.Barbata, oysters each 30 grams, rhubarb, cooked Aconite (2) 20 grams, add water to cook, to the residue. Retention enema the day 1-2 doses.(3) oliguria desirable 30 g Plantago cloth Jianzhi, then add the stems m 100 g taken with Zhu Chengyu.(4) polyuria bow desirable black beans 500 grams, longan meat 15 grams, jujube 50 grams, add water, a total mess a day, morning and evening hours of service.(5) urine of desirable 3 grams of ginseng 3, walnut meat, boiled for one hour, Yin Tang to eat parameters and meat.(6) the escargot 5-7 peeled smashed deposited Guanyuan.(7) fresh car before the grass 60 grams, 60 grams of Xianou Daozhi once served.Abduction Bo (8) 12 grams, 30 grams of long-nosed pit viper, tongue grass, Scrophulariaceae 30 grams, decoction hot compress.

Complications of renal failure - chronic renal failureChronic renal failure is often complicated by high blood pressure, anemia, heart failure, pericarditis, cardiomyopathy, hydropower disorders and acid-base imbalance, renal osteodystrophy, fractures, infections, etc.. In addition to the above complications, chronic renal failure of long-term dialysis can also be complicated by aluminum toxicity, and regular dialysis treatment of ESRD patients may predispose to aluminum toxicity. Regularity hemodialysis patients with aluminum intoxication lead to chronic renal failure for many reasons, including: excessive aluminum content of dialysis fluid. When dialysate aluminum content close to 50μg / L, a high incidence of aluminum-related bone disease. Therefore, the authors suggest that the aluminum content in dialysis fluid should be at least less than 10μg / L, preferably less than 5μg / L. The kidney is the only way to rows of aluminum, aluminum absorption in chronic renal failure in the in vivo accumulation of of Erzhi aluminum poisoning. End stage renal disease in patients with aluminum excretion is blocked, more emphasis on the accumulation of aluminum in the body, the body of aluminum content can be 20 times higher than normal. The largest organ of aluminum accumulation in bone, liver and spleen. The increased content of aluminum to aluminum toxicity, aluminum-related bone disease can lead to bone. Aluminum were deposited mainly in the edge of the calcification of bone, mineralized bone and unmineralized at the interface of the young bone, causing osteomalacia. Osteomalacia histological changes in the extent of aluminum deposition in the edge of the calcified bone. Aplastic bone disease may be a prelude to the aluminum-induced osteomalacia. Aplastic bone disease was first reported in 1982, a renal osteodystrophy. Now think that this is a major bone lesions of chronic renal failure, peritoneal dialysis patients. Some cases are caused by excessive aluminum accumulation but too much inhibits parathyroid hormone may be more important reason. Parathyroid hormone plays an important role in maintaining normal bone metabolism. Parathyroid hormone by increasing bone transport to prevent the deposition of aluminum in the mineralization of the leading edge of parathyroidectomy occurrence of aluminum-related bone disease is a risk factor that can reduce bone formation rate and update rate aluminum accumulation in the calcified bone edge, thereby interfering with the bone mineralization process. Clinically, the aluminum-related bone disease should be excluded before considering to do parathyroidectomy in secondary hyperparathyroidism, as a reduction in parathyroid hormone levels can accelerate the coexistence of osteomalacia in patients with aluminum deposition in bone and accelerate aluminum the occurrence of bone disease. Past reports of aluminum-related bone disease incidence rate was as high as 15% to 25%. In recent years, noting that the limit of aluminum-containing phosphorus binders to use and improve the handling of the dialysis fluid, the incidence rate has decreased significantly.
Renal failure - diet adjustmentBooks in patients with chronic renal failure renal failure diet regulation is a very important part of treatment principles, often seen in clinical diet inadvertently lead to disease progression or death case.Should be soft diet and avoid hard foods and fried foodsPatients with chronic renal failure due to toxin retention in the body and blood microcirculatory disturbance and other reasons caused by the gastrointestinal mucosa often has congestion, erosion status, such as eating solid food, fried foods such as sesame cake sugar, fried noodles nest, often leading to food stomach pierced the blood vessels and cause bleeding. Due to chronic renal failure in patients with uremia coagulation disorders, bleeding difficult to stop, it will lead to death.Second, the diet should be light, avoid spicy spicy foodChronic renal failure, uremic patients with gastrointestinal mucosa often has congestion, erosion status, such as eating hot peppers, white wine and other spicy food, often add to the erosion of the gastrointestinal mucosa, resulting in the bleeding of the stomach lining of blood vessels.

Renal failure - food taboos
Renal failure in patients with renal failure diet precautions:Kidney dysfunction, unable to urinary toxins excreted and accumulate in the blood poisoning symptoms (ie, uremia), will cause the body has too much hydrogen, sodium and potassium.Control diet, is a basic treatment for patients with chronic renal failure, can reduce the production of toxins in urine, and also to maintain the body's minimum demand for nutritional and electrolyte balance, however, this plan is required to patients and their families efforts to overcome a challenge, because it is often necessary to give up some food to satisfy their appetites.The principles of the diet:An adequate protein intake;2, adequate intake of calories;3, pay attention to controlling water and salt (sodium) intake;4, avoid foods containing high potassium and phosphorus.An intake of high quality proteinRenal failure patients should limit protein intake, in order to reduce the burden on the kidneys, but eat less, consume the body's muscles and splanchnic tissues, it is necessary to eat the correct and sufficient "quantity" and "quality" protein, the amount of should be 1 to 1.2 grams per kilogram of body weight per day, intake of high value, high quality physiological animal protein foods, such as: milk, eggs, meat. Produce more nitrogen-containing waste due to lower utilization of plant proteins in the body, metabolism, and so can not be safe to eat, such as: beans (red beans, mung beans, peas, broad beans, soybeans, peas, nuts), soy products ( tofu, dried tofu, soy milk), gluten products (wheat gluten, flour, intestinal, baked bran), nuts (seeds, peanuts, walnuts, cashew, chestnut). Vegetarian soy products and cereals contain essential amino acids is not complete, in order to improve the protein utilization of vegetarians, these foods to be together with food, can play a complementary effect; the best change to eat custard factors is appropriate. protein intake by quantitative standards.Second, adequate intake of calories
Low-protein, starch, protein restriction, in order to avoid the lack of caloric intake, will increase the production of nitrogenous waste, eat more high-calorie and very low protein food supplement. Vegetable oil (such as: soybean oil, peanut oil), low-protein starch (such as: Cheng powder, white powder, lotus root starch) and carbohydrates (such as: rock candy, honey, ginger candy, fruit sugar) to produce a variety of delicious snacks, the heat intake per day, 30 to 40 kcal per kilogram of body weight to avoid weight loss over even.Third, careful control of moistureWhen kidney failure and decreased urine output, water will accumulate in the body, increased load on the cardiovascular system, no vitality, edema, weight gain, cough, lie down and shortness of breath, lower hematocrit (Hct), and concurrent high blood pressure, heart failure, pericarditis, and dialysis due to dehydration is a drastic one, prone to headaches, nausea, vomiting, muscle cramps imbalance syndrome. Daily weight gain is limited to no more than one kilogram of water intake for the day before the total urine output plus 500 to 700 milliliters (ml). If the first day urine output was 500ml, 500cC +500 at (7D0) ml = 1000 ~ 1200ml, that is, throughout the day to drink the water, including water, porridge, milk, soup and drinks. Avoid drinking mostly water, ice water mouthwash, chewing gum or squeeze a little lemon juice to reduce the sensation of thirst, try taking the time to focus on consumption, reduce the amount of water to the soup.Fourth, pay attention to the control of saltRenal failure can not be discharged to water, salt, easily lead to edema and increased blood pressure. Patients should not be a day more than the consumption of 5 grams of salt. 1 gram (1/5 of tea soup) salt = 6/5 of tea soup soy sauce = 1 tea soup MSG, so the above seasoning contains salt do not feel free to add; can be used instead of sugar, onions, ginger, garlic to improve the taste. And should be limited to high-sodium foods such as processed canned, salted and smoked products, Lay sauce, pickles, pickled vegetables and fast food. Loss of appetite, without salt restriction, to be able to eat the nutritious for the former title, wait for a good appetite, nutritionally adequate, and then limit the salt.
Kidney five beware of high potassiumPotassium ions can not be excreted by the kidneys of the severely damaged, can cause hyperkalemia "may cause numbness of the fingers, fatigue, weakness, chest, nausea, stiff tongue, difficulty speaking, loss of consciousness, serious arrhythmia or cardiac arrest.Hyperkalemia reasons: one, inadequate dialysis;, no appetite;, constipation; 4, the intake of high potassium foods, high potassium vegetable, to go to Peel and cut into small pieces, with plenty of clean boiled ~~ 5 minutes picked up, and then mix in oil or fried; the potassium content of coffee, tea, chicken, and the concoction of the high cause hyperkalemia.
High potassium vegetables: green leafy vegetables (such as spinach, water spinach, amaranth, lettuce), mushrooms, seaweed, kelp, carrots, potatoes.
Potassium fruits: bananas, tomatoes, dates, oranges, oranges, mangoes, persimmons, cantaloupe, grapefruit, carambola (easy to burp), it is recommended each time a fruit-based, weight about 1/6 is appropriate.

Low potassium fruits: pineapple, papaya, watermelon, pear, strawberry, lemon, etc., but not Yichi.To maintain the balance of calcium and phosphorusCalcium and phosphorus are important minerals in the body, the two can maintain a good growth of bones and teeth, and neuromuscular normal operation. Calcium is insufficient, to be more fresh milk, calcium and vitamin D can reduce the occurrence of renewal hyperparathyroidism. Phosphorus commonly found in all protein-containing food, to adequate nutritional intake, but also reduce the absorption of phosphorus, only when eating and to chew taking aluminum hydroxide, calcium carbonate and other phosphate binders to combine food phosphorus. Note the high phosphorus foods: whole grains and products (such as brown rice, embryo rice, whole wheat bread), visceral (liver, kidney, brain), stone fruits (peanuts, cashews, walnuts) and butter products (peanut butter), chocolate, egg yolk, milk, dairy intake.Less consumption of aluminum-containing and purine foods to avoid aluminum poisoning and gout.High aluminum diet: tea, cheese, tea, steamed sponge cake, cooking in aluminum containers.
High purine diet: gravy, lentils, thick broth, lean meat, duck, brain class, mushrooms, offal (liver, kidney, heart), sardines, eels class, asparagus.

Renal failure - diagnostic methodsAcute renal failure can change according to the history of the primary disease, oliguria and urine characteristics make the diagnosis. But it should be functional (prerenal) oliguria phase identification, the above-mentioned blood and urine tests can identify funding, but in practical work, and more with fluids or mannitol, furosemide, a diuretic test to help determine. 30-40min intravenous infusion of 10% glucose 500ml, such as volume increases (39-50ml / h), functional oliguria (heart dysfunction, hanged the Act); hypovolemia has been corrected or no urine road obstruction, can be used 20% mannitol 100-125ml intravenous injection, 15min end note, or intravenous furosemide 80-320mg, 2 hours, urine output remains <40ml, acute renal failure may be considered to have been formed. Conditional, central venous pressure determination, such as <588.42pa, should be of their blood volume before the injection of mannitol or furosemide.Renal failure - treatment methodsRenal failure patients, the treatment result in kidney failure, such as lack of blood supply or blood loss, will be given to patients to replenish lost body fluids and water; further treatment for infection if there is infection.

2, due to the kidney has lost its function, so the physician will be the temporary use of dialysis treatment (commonly known as kidney dialysis), to help rid the body of toxins and waste; patients with acute renal failure Failure to receive appropriate treatment or can not control the disease from acute evolve into chronic renal failure may be due to uremia must be life-long dialysis.Diet for patients with kidney failure, renal damage, food to eat into the body, toxins and waste can not be excreted normally, and therefore must pay special attention to diet, to avoid body burden:a, protein restriction: non-dialysis patients, because the kidneys can not protein metabolism resulting from waste discharge, renal failure, the situation is more serious, therefore, proposed to reduce the intake of protein; but if so, when the dialysis, It should be noted, will result in the loss of body protein in dialysis, it is necessary to meet the nutritionist's advice, in order to maintain the body needs.b, limiting sodium intake: the salt contains a high sodium content, if too much sodium in patients with renal failure in vivo, can cause the body of water retention, which causes heart and lung failure and renal failure aggravated the situation. Do not use low sodium due to low sodium, high in potassium.c, the restriction of potassium intake: the accumulation of potassium can cause muscle weakness, severe cases can cause arrhythmia and cause the generation of heart failure.d, to limit phosphorus intake: body of excessive phosphorus cause calcium loss, so the doctors will use drugs to help control the phosphorus content of the blood to prevent the generation of osteoporosis.e, water intake: excessive consumption of water, occurs when the kidneys can not exclude edema or cause heart and lung failure, so moisture control is a very important issue, the doctor will be a case the amount of urine, or The dialysis exclude the amount of water to determine the amount of water intake, the general will follow the previous day's urine output plus 500-750c.c.
4, renal transplantation: some late renal failure patients requiring long-term dialysis treatment, patient conditions are suitable kidney transplant (kidney transplant) for patients with a better quality of life; but a kidney transplant is a big project, though current medical technology has been quite good, and still do a lot of ex ante assessment, in order to improve the probability of transplant success.Kidney if kidney damage is still at an early stage, you can rely on medication and diet control, however, end stage renal failure kidney transplant surgery, organ donor kidney transplanted into the patient's body accept the transplant process. Possible sources of the kidney: family, spouse, close friend, or brain death and during his lifetime signature to agree to organ donation. Of course, the best match of the kidney is usually from the transplant recipient brothers and sisters, because their genes with the most likely.

Kidney transplantation is the treatment of kidney failure, the best way, because transplanted to the kidney of the patient's body is almost completely replace the function of kidney failure, and allow patients to lead a normal life.
Unfortunately, not every renal failure patients have the opportunity to receive a kidney transplant. This may not be suitable for kidney or relatives willing to donate kidneys, and then, or because the number of organ donors after brain death is far less than the number of demand. Patients have to wait until a suitable kidney for renal transplantation to take a very long period of time, because kidney donors must be with the patient's body to match. At this time, the patient must be regular dialysis treatment to sustain life until you can get a new kidney transplant.

Dialysis is by filtering, to selectively exclude certain substances in the blood. In other words, by artificial means to patients in renal failure after in vivo accumulation of toxic waste, water and salt ruled out, so that the physical condition of the patient back to health.Currently used in kidney dialysis in two forms: hemodialysis and peritoneal dialysis. Hemodialysis using a special machine to replace kidney function. Peritoneal dialysis the peritoneum of the human body acts as a filter and remove toxins.

Renal failure - prevention methods
The various causes of renal failure patients with chronic kidney disease, often showing irreversible renal damage, until the development of end stage renal failure. Chronic renal failure in the early prevention of significant, very important, the so-called early prevention, also known as "primary prevention" refers to the intervention treatment in chronic renal failure before the relevant factors, including the following aspects:

(1) aggressive treatment of primary disease on a variety of acute, chronic glomerulonephritis, lupus nephritis, purpura nephritis, or kidney may be involved in diseases (such as hypertension, diabetes), active treatment, to prevent the occurrence of chronic renal failure .

(2) to avoid or eliminate some risk factors for the application of kidney toxic drugs, serious infections, dehydration, urinary tract obstruction (such as stones, benign prostatic hyperplasia), trauma and other factors, often can make the heavier of the original kidney disease, renal deteriorated, prompting renal failure. In fact, recurrent, high-quality follow-up time, can reduce or avoid these risk factors occur, early detection and correct.

(3) a reasonable program of diet low in protein, low phosphorus and low-fat diet, the renal protective effect of chronic kidney disease has been confirmed by laboratory and clinical. It is stressed that in order to prevent the occurrence of chronic renal failure, serum creatinine 159.1 micro mol / l should limit protein intake.

(4) of the angiotensin converting enzyme inhibitors can not only control of systemic hypertension, but also to correct glomerular hyperperfusion, hyperfiltration state, delay renal failure occurred. Clinical drug Captopril, Lotensin, and profit pressure,.