Acute renal failure

　　Acute renal failure is a clinical syndrome characterized by a rapid decrease in renal excretory function due to various causes, leading to severe disorder of the internal environment of the body. Clinically, it is mainly manifested as azotemia, hyperkalemia, and metabolic acidosis, and is often accompanied by oliguria or anuria. Acute renal failure can be divided into three major categories according to the cause: pre-renal, renal, and post-renal. The following experts introduce the etiology of acute renal failure.

　　I. Pre-renal acute renal failure

　　Pre-renal acute renal failure is caused by a sharp decrease in renal blood perfusion and is common in the early stage of shock. At this time, a decrease in effective circulating blood volume and a decrease in blood pressure not only directly lead to a decrease in renal blood flow but also cause strong constriction of renal arterioles through the sympathetic-adrenal medulla system and the renin-angiotensin system, further reducing renal blood perfusion and effective filtration pressure. Therefore, GFR significantly decreases. At the same time, an increase in secondary aldosterone and ADH secretion can enhance the reabsorption of sodium and water by the distal tubules and collecting ducts, resulting in a significant decrease in urine output, a urine sodium content below 20 mmol (mEq)/L, and a higher urine specific gravity. The sharp decrease in GFR can also cause hyperkalemia and acid-base imbalance.

　　Since there is no organic damage to the renal parenchyma in the pre-renal acute renal failure, when blood volume, blood pressure, and cardiac output return to normal due to timely treatment, renal urinary function also returns to normal immediately. Therefore, it is generally considered a functional acute renal failure, but if renal ischemia persists for too long, it can cause organic damage to the kidneys, leading to renal acute renal failure.

　　II. Renal acute renal failure

　　Acute renal failure caused by organic lesions of the kidney is called renal acute renal failure. For example, acute glomerulonephritis and lupus nephritis (seen in systemic lupus erythematosus) can cause dysfunction of a large number of glomeruli due to inflammatory or immunological damage, thus leading to acute renal failure. Bilateral renal artery embolism can also cause acute renal failure. In addition, acute pyelonephritis, eclampsia,结节性多动脉炎 (nodular polyarteritis) and other conditions can also cause acute renal failure. However, the most common in clinical practice is acute renal failure caused by acute renal tubular necrosis due to renal ischemia and nephrotoxins. The causes of acute renal tubular necrosis are divided into two categories.

　　1, Renal ischemia is more common in cases of shock caused by various reasons and when timely and effective rescue is not provided. At this time, severe and sustained hypotension and strong constriction of renal arterioles can significantly and continuously reduce renal blood perfusion. Therefore, ischemic damage to the renal tubules can occur, even leading to necrosis. After the occurrence of renal tubular organic lesions, even if the blood volume is corrected and blood pressure is restored to normal, the renal urinary function cannot be restored rapidly. The patient's urine contains protein, red and white blood cells, and various casts. The concentration of urine sodium generally increases to 40-70 mmol (40-70 mEq)/L or higher, indicating that the renal tubules have lost their sodium conservation function due to damage.

　　2, Nephrotoxic heavy metals (mercury, arsenic, antimony, lead), antibiotics (dicloxacillin, neomycin, polymyxin, gentamicin, cefalosporins, etc.), sulfonamides, certain organic compounds (carbon tetrachloride, chloroform, methanol, phenol, toluene, etc.), insecticides, and poisonous mushrooms. Certain vascular and renal contrast agents, snake venom, myoglobin, and other substances excreted by the kidneys can directly damage the renal tubules, even causing necrosis of renal tubular epithelial cells. At this time, if there is insufficient renal blood perfusion, it will further exacerbate the damage to the renal tubules.

　　Under many pathological conditions, renal ischemia and nephrotoxins often act simultaneously or sequentially. For example, during the action of nephrotoxins, local vasoconstriction can occur in the kidney, leading to renal ischemia; conversely, renal ischemia is often accompanied by the accumulation of toxic metabolic products. It is generally believed that when renal ischemia is combined with the action of nephrotoxins, it is most likely to cause acute renal failure.

　　Acute renal failure caused by acute tubular necrosis. Clinically, it can be divided into oliguric type and non-oliguric type according to whether there is oliguria. The oliguric type is more common, with sudden onset of oliguria (urine output less than 400ml in 24 hours in adults) or even anuria (urine output less than 100ml in 24 hours). Non-oliguric type patients do not have a decrease in urine output, and even can increase, but azotemia becomes more severe day by day, accounting for about 20% of this type.

　　Three, post-renal acute renal failure

　　Any urinary tract obstruction from the renal pelvis to the urethral orifice can cause post-renal acute renal failure. Obstruction above the bladder is often caused by stones. However, due to the strong compensatory reserve function of the kidneys, post-renal acute renal failure is only caused when both sides of the urinary tract are obstructed simultaneously or one kidney has lost function while the other urinary tract is blocked. Obstruction of the bladder and urethra can be caused by bladder dysfunction (such as chronic urinary retention caused by spinal cord atrophy, diabetic pseudosclerosis, etc.) or benign prostatic hyperplasia, prostatic cancer, and others.

　　In the early stage of post-renal acute renal failure, there is no organic damage to the renal parenchyma. Timely relief of obstruction can quickly restore renal urinary function. Therefore, for such patients, early diagnosis and appropriate treatment should be given.

　　Acute renal failure usually goes through three stages of development: oliguria phase (or anuria phase), polyuria phase, and recovery phase. The main complications that may occur during the oliguria phase of acute renal failure are:

　　One, infection is one of the most common and severe complications, often seen in severe trauma, burns, and other causes of hypermetabolic acute renal failure.

　　Two, complications of the cardiovascular system include arrhythmia, heart failure, pericarditis, hypertension, and others.

　　Three, complications of the nervous system include headache, drowsiness, muscle twitching, coma, epilepsy, and are related to the retention of toxins in the body, water intoxication, electrolyte disorders, and acid-base imbalance.

　　Four, complications of the digestive system are manifested as anorexia, nausea, vomiting, abdominal distension, hematemesis, or hematochezia, and bleeding is often caused by erosion of the gastrointestinal mucosa or stress ulcers.

　　Five, complications of the blood system due to the rapid decline in renal function can lead to a decrease in erythropoietin, thus causing anemia, but most cases are not severe. A few cases may have a tendency to bleed due to a decrease in coagulation factors.

　　Six, electrolyte disorders and metabolic acidosis can lead to hyperkalemia, hyponatremia, and severe acidosis, which are one of the most dangerous complications of acute renal failure.

　　During the polyuria phase, the patient's daily urine output can reach 3000-5000ml. Due to the excretion of a large amount of water and electrolytes, dehydration, hypokalemia, hyponatremia, and other conditions may occur. If not supplemented in time, the patient may die of severe dehydration and electrolyte disorder.

　　During the recovery phase, the levels of serum urea nitrogen and creatinine return to normal, uremic symptoms disappear, renal tubular epithelial cells regenerate and repair, and the renal function of most patients can be completely restored. A few patients may have varying degrees of renal function damage.

　　According to the degree of urine reduction, acute renal failure can be divided into oliguric and non-oliguric types. Acute renal failure with oliguria or anuria is called oliguric type. Non-oliguric type refers to a rapid increase in blood urea nitrogen and creatinine, and a rapid decrease in creatinine clearance without oliguria; clinical common oliguric acute renal failure, the clinical process is divided into three stages:

　　(I) Oliguria phase

　　The oliguria phase generally lasts 1-2 weeks, and longer cases can last up to 4-6 weeks. The longer the duration, the more severe the renal damage. Those with oliguria for more than 5 days or anuria for more than 10 days have poor prognosis. The systemic symptoms of the oliguria phase include:

　　1. Water and sodium retention

　　Children may present with systemic edema, hypertension, pulmonary edema, cerebral edema, and heart failure. Sometimes, due to water retention, hyponatremia with hygroscopic properties may occur.

　　2. Electrolyte disorder

　　Commonly found are hyperkalemia, hyponatremia, hypocalcemia, hypermagnesemia, hyperphosphatemia, and hypochloremia.

　　3. Metabolic acidosis

　　Manifested by nausea, vomiting, fatigue, drowsiness, deep and rapid breathing, anorexia, and even coma, with a decrease in blood pH value.

　　4. Uremia

　　Due to renal excretion disorders, various toxic substances accumulate in the body, which can cause systemic symptoms of poisoning. The severity is consistent with the concentration of blood urea nitrogen and creatinine.

　　(1) Digestive system: Manifested as anorexia, nausea, vomiting, diarrhea, and in severe cases, digestive hemorrhage or nitrogen, while gastrointestinal bleeding can exacerbate azotemia.

　　(2) Cardiovascular system: Mainly caused by water and sodium retention, manifested as hypertension and heart failure, and may also occur arrhythmias, pericarditis, etc.

　　(3) Neurological symptoms: There may be drowsiness, confusion, anxiety, convulsions, coma, and autonomic nervous system disorders such as excessive sweating or dry skin, which can manifest as various functional disorders such as consciousness, behavior, memory, sensation, and emotion.

　　(4) Hematological system: APF is often accompanied by normocytic normochromic anemia, which worsens with the deterioration of renal function. This is due to a decrease in red blood cell production, extravascular hemolysis, blood dilution, and gastrointestinal bleeding. Bleeding tendency (gum bleeding, nosebleeds, skin petechiae, and gastrointestinal bleeding) is often caused by thrombocytopenia, platelet dysfunction, and DIC. The total white blood cell count is often elevated in the early stage of acute renal failure, and the proportion of neutrophils also increases.

　　5. Infection

　　Infection is the most common complication of ARF, with respiratory and urinary tract infections being more common, and the most common pathogenic bacteria are Staphylococcus aureus and Gram-negative bacilli.

　　(II) Polyuria phase

　　When the urine output of ARF patients gradually increases, systemic edema subsides, and the 24-hour urine output reaches above 250ml/m2, it is considered the diuretic phase, which generally lasts 1-2 weeks (longer cases can last up to a month). During this period, due to excessive urination, dehydration, hyponatremia, and hypokalemia may occur. Early azotemia may persist or even worsen, while renal function gradually recovers in the later stage.

　　(Three) Recovery period

　　After the diuretic period, the renal function improves, urine output returns to normal, blood urea nitrogen and creatinine levels gradually return to normal, but the renal concentration function needs several months to return to normal, and a few patients may have some irreversible renal function damage. During this period, children may present with weakness, emaciation, malnutrition, anemia, and low immune function.

　　ATN caused by nutrition is mostly non-oliguric acute renal failure, with mild symptoms of acute renal failure, fewer complications, and a low mortality rate.

　　The prevention of acute renal failure mainly focuses on the active prevention and treatment of the primary disease, and avoiding and eliminating the precipitating factors is the fundamental of prevention. Therefore, the following three points should be paid attention to:

　　One, nourishing the five internal organs: live a regular life, have a regular diet, pay attention to hygiene, avoid external evil invasion, especially in the season and region of epidemic diseases, more preventive measures should be strengthened; do not overeat spicy, hot, and greasy foods to avoid the production of damp-heat; regulate one's emotions, maintain a cheerful spirit, and keep the Qi and blood flowing smoothly to avoid Qi stasis and blood stasis; strengthen physical exercise, and improve the body's defense ability.

　　Two, prevent poisoning: Relevant data show that 20% to 50% of acute renal failure is caused by drugs, and some are due to exposure to harmful substances. Therefore, it is necessary to avoid using and contacting drugs or toxins that are harmful to the kidneys as much as possible. If accidental ingestion or contact occurs, it should be discovered and treated as soon as possible.

　　Three, timely prevention and treatment: Once the primary disease that induces acute renal failure occurs, it should be treated early, with attention to expand blood volume, correct water and electrolyte imbalance, and acid-base imbalance, and restore circulatory function. If the onset of the disease is found, early measures should be taken to supplement blood volume, increase cardiac output, restore renal perfusion and glomerular filtration rate, remove renal tubular obstruction, prevent infection, and prevent renal parenchymal damage caused by DIC and renal ischemia. At the same time, the application of blood circulation and blood stasis drugs should be started as soon as possible, which has a positive effect on preventing the occurrence of the disease.

　　Acute renal failure, abbreviated as ARF, is a clinical critical illness. This disease is an acute renal injury caused by various etiologies, which can cause a rapid decrease in the regulatory function of renal units within a few hours to a few days, leading to the inability to maintain fluid and electrolyte balance and excrete metabolic products, resulting in hyperkalemia, metabolic acidosis, and acute uremic syndrome. This syndrome is clinically known as acute renal failure. So, what kind of laboratory tests should be done for acute renal failure? The following expert introduces the laboratory tests that need to be done for acute renal failure.

　　1. Blood examination

　　There is mild to moderate anemia. Blood creatinine and blood urea nitrogen levels progressively increase, and if combined with hypermetabolism and rhabdomyolysis, the rate of increase can be faster, leading to hyperkalemia (greater than 5.5 mmol/l). The blood pH value is often below 7.35, and the HCO3[supclass="normal"]-[/sup] level is often slightly to moderately decreased. Blood sodium concentration is normal or slightly low, and there may be decreased blood calcium and increased blood phosphorus.

　　2. Urine examination

　　① Urine volume change: oliguria or anuria often suggests ATN. ② Urinalysis: the appearance is often turbid, and the urine color is deep. Urinary protein is mostly - to +, usually dominated by middle and small molecular proteins. Urine sediment can see renal tubular epithelial cells, epithelial cell casts, and granular casts, and a few red and white blood cells can be seen, and the urine specific gravity is often below 1.015. ③ Urine osmolality is below 350 mOsm/kg, and the ratio of urine to blood osmolality is below 1.1. Due to the reduced reabsorption of sodium by the renal tubules, urinary sodium increases, usually between 20 to 60 mmol/l; the ratio of urinary creatinine to blood creatinine decreases, often below 20; the ratio of urinary urea nitrogen to blood urea nitrogen decreases, often below 3; the renal failure index is often greater than 1; the sodium excretion fraction is often greater than 1.

　　3. Imaging examination

　　B-ultrasound examination is the most commonly used. During acute renal failure, the kidney volume often increases, and the renal cortex can thicken, while during chronic renal failure, the kidney volume often decreases, and the renal cortex becomes thin. In addition, ultrasound examination can also help to differentiate whether there is post-renal obstruction, and in cases of upper urinary tract obstruction, both upper segments of the ureters can be dilated or both renal pelvises can have hydrops, while in cases of lower urinary tract obstruction, bladder urine retention can be seen. Abdominal X-ray films, intravenous or retrograde pyelography, CT, or magnetic resonance imaging are usually helpful in finding the exact cause of suspected urinary tract obstruction.

　　4. Renal biopsy

　　It is an important diagnostic method. For patients with typical clinical manifestations of ATN, renal biopsy is generally not necessary. For patients with clinical manifestations consistent with ATN, but with oliguria exceeding 2 weeks or unknown etiology, and renal function not recovering within 3-6 weeks, clinical consideration should be given to the existence of other serious renal parenchymal diseases that cause acute kidney injury, and renal biopsy should be performed as soon as possible to facilitate early etiological diagnosis.

　　Patients with acute renal failure require sufficient calories. The supply of calories should be mainly from easily digestible carbohydrates, and fruits can be used more, with wheat starch noodles, wheat flakes, biscuits, or other wheat starch desserts, adding a small amount of rice soup or thin gruel. For patients with acute renal failure, 15 to 20 grams of high biological value and low protein diet should be provided daily during the oliguria period, which takes into account both the patient's reduced excretory capacity due to renal insufficiency and the patient's nutritional needs.

　　If the duration of oliguria is prolonged, widespread trauma, or extensive burns result in significant protein loss, in addition to supplementing with high biological value and low protein, it is also advisable to consider elemental diet. The amount of protein supply can gradually increase with the decrease of blood non-protein nitrogen. High biological value protein should account for 1/2 to 1/3 of the total protein, and food rich in essential amino acids such as milk and eggs can be selected. During the oliguria period, fluid intake should be limited to prevent excessive body fluid leading to acute pulmonary edema and dilutional hyponatremia. The water content in food (including rice and steamed buns) and the water produced by oxidation should also be calculated (fats produce more water, while proteins and carbohydrates produce less). In the case of properly calculated fluid intake, various fresh fruits or vegetable juices can be consumed to provide vitamins such as vitamin C and inorganic salts.

　　Pay attention to the intake of sodium and potassium: because patients with acute renal failure often have edema and are prone to hyperkalemia, it is necessary to adopt a low-salt, salt-free, or low-sodium diet according to the degree of edema, the amount of urine, and the results of blood sodium determination. If blood potassium levels rise, reduce the amount of potassium in the diet to avoid exacerbating hyperkalemia due to increased exogenous potassium. Since potassium is present in all kinds of food, in addition to avoiding foods with high potassium content, methods such as freezing, soaking in water, or discarding the soup can be used to reduce potassium content.

　　1. Foods suitable for patients with acute renal failure

　　Foods suitable for patients with acute renal failure: Milk, eggs, lean meat, wheat starch noodles, wheat flakes, biscuits, or other wheat starch desserts, fruit juice, tea, green vegetable water, fruits, vegetables, etc.

　　Foods suitable for patients with acute renal failure: During oliguria, glucose, sucrose, fresh lemon juice, etc. can be used; during polyuria, various beverages such as fruit juice, tea, cocoa, green vegetable water, etc. can be used.

　　2. Foods to avoid for patients with acute renal failure

　　Limit the intake of eggs, milk, and other foods according to the condition; limit water intake; avoid the use of fatty and high-protein foods. Limit the intake of milk, eggs, or lean meat according to the condition; avoid irritant foods such as alcohol, coffee, and chili.

　　The treatment principle of acute renal failure is to remove the cause, maintain water, electrolyte and acid-base balance, alleviate symptoms, improve renal function, and prevent complications. Whether it is pre-renal or post-renal, electrolyte and acid-base balance should be maintained at the same time as fluid replacement or obstruction removal. There are also unique methods for treating acute renal failure in traditional Chinese medicine. The following experts introduce the treatment methods of acute renal failure in traditional Chinese medicine.

　　Firstly, oliguric stage

　　1. Exuberant syndrome of evil heat: Sudden decrease in urine output, even obstruction, persistent fever, dry mouth and a desire for drinks, constipation, restlessness and anxiety, red tongue with purple spots, yellow and dry coating, rapid pulse. Drain fire and detoxify. Modified Dachengqi decoction.

　　2. Deficiency of both Qi and Yin: Shortness of breath, weakness in the waist and knees, hot palms and soles, dry mouth and a desire for drinks, or dry mouth without a desire for much drinking, slightly red tongue with notches, thin coating, deep, thin, and rapid pulse. Tonify Qi and nourish Yin. Maiwei Dihuang decoction with ginseng and huangqi, etc.

　　Secondly, Acupuncture Therapy

　　Firstly, needle the Qihai, Tianchi and other acupoints 3-7 times, and then take internal medications such as Liushisan powder to promote urination. Moxibustion at the Shenshu and costovertebral angle can sometimes increase urine output.