Pediatric acute renal failure

　　First, etiology

　　APF can be divided into pre-renal (accounting for about 55%), renal (accounting for about 40%), and post-renal (accounting for about 5%) according to etiology.

　　1. Pre-renal

　　Acute renal failure occurs due to decreased renal perfusion and GFR, which is restored to normal after the cause is eliminated due to the absence of organic damage to the kidneys.

　　(1) Hypovolemia: such as massive hemorrhage, fluid loss from the gastrointestinal tract (such as diarrhea, vomiting, gastrointestinal decompression), fluid loss from the kidneys (such as osmotic diuresis, diuretics, adrenal insufficiency), skin loss (such as burns, excessive sweating), third space fluid loss (such as pancreatitis, peritonitis, extensive injury with crush injury).

　　(2) Decreased cardiac output: cardiogenic shock, congestive heart failure, pericardial tamponade, massive pulmonary embolism.

　　(3) Systemic vasodilation: allergic reactions, the use of antihypertensive drugs, sepsis, and excessive use of vasodilatory drugs.

　　(4) Systemic or renal vascular constriction: anesthesia, major surgery, α-adrenergic agonists or high-dose dopamine, hepatorenal syndrome.

　　(5) Disturbance of renal autoregulation: such as the use of non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors.

　　2. Renal

　　Decreased GFR is caused by tubular cell damage (acute tubular necrosis) due to low perfusion or renal toxic substances, glomerular, interstitial or vascular inflammation, thrombosis leading to embolic renal vascular obstruction or vasomotor nephropathy (vasomotornephropathy).

　　(1) Acute tubular necrosis:

　　① Acute renal ischemia: such as trauma, burns, major surgery, massive hemorrhage, severe salt loss, dehydration, acute hemoglobinuria, acute myoglobinuria, Gram-negative bacillary sepsis, etc., can all cause renal ischemia and hypoxia leading to acute tubular necrosis.

　　② Renal toxic substance injury: substances that cause tubular toxicity and necrosis include:

　　A, Exogenous: such as antibiotics (such as aminoglycosides, cephalosporins, tetracyclines, amphotericin B, vancomycin, polymyxin, etc.); X-ray contrast agents; heavy metals (such as mercury, lead, arsenic, bismuth, etc.); chemotherapeutic agents (such as cisplatin, methotrexate, mitomycin); immunosuppressants (such as cyclosporine); organic solvents (such as ethanol, carbon tetrachloride); pesticides; fungicides; biological toxins (such as snake venom, scorpion venom, bee venom, fresh fish bile, toxic mushrooms, etc.).

　　B, Endogenous: such as rhabdomyolysis, hemolysis, uric acid, oxalate, hypoproteinemia (such as myeloma).

　　(2) Acute glomerulonephritis and/or vasculitis: post-streptococcal glomerulonephritis, rapidly progressive glomerulonephritis, pulmonary hemorrhagic nephritis syndrome, acute diffuse lupus nephritis, purpura nephritis, etc.

　　(3) Acute interstitial nephritis: infection变态反应, drug变态反应 (such as penicillin group, sulfonamides, analgesics, or non-steroidal anti-inflammatory drugs, etc.), infection itself (such as epidemic hemorrhagic fever, etc.).

　　(4) Acute renal parenchymal necrosis: acute renal cortex necrosis, acute renal medulla necrosis.

　　(5) Renal vascular diseases: necrotizing vasculitis, allergic vasculitis, malignant hypertension, renal artery thrombosis or embolism, bilateral renal vein thrombosis. Sepsis can also cause disseminated intravascular coagulation (DIC), leading to acute renal failure.

　　(6) Others: acute rejection of transplanted kidneys, etc.

　　3, Post-renal

　　Obstruction of the urinary tract below the kidney causes hydronephrosis, increased interstitial pressure, and damage to the renal parenchyma due to compression. Over time, it causes reflex constriction of the renal blood vessels, leading to ischemic damage to the kidney. If accompanied by secondary infection, it will further worsen the damage.

　　(1) Urethral obstruction: urethral stricture, congenital valve, phimosis, trauma from being stepped on, and urethral injury.

　　(2) Bladder neck obstruction: neurogenic bladder, stones, tumors, blood clots.

　　(3) Ureteral obstruction: congenital narrowing of the ureter, stones, blood clots, or detachment of necrotic renal tissue (papilla), tumor compression, retroperitoneal fibrosis.

　　Second, Pathogenesis

　　The physiological functions of the kidneys include excretion (filtration and reabsorption), regulation of water, electrolytes, and acid-base balance, as well as endocrine metabolism. These aspects of function are complementary and closely related. When the glomerular filtration rate (glomerular filtration rate, GFR) decreases to below 50% of the normal level, the serum creatinine quickly rises to >176mol/L (2.0mg/dl), BUN also increases, and it leads to disturbance of water, electrolyte, and acid-base balance, causing acute uremic symptoms, which is known as ARF.

　　1, Pathological changes

　　(1) Gross examination: the kidneys are enlarged and soft in texture. When the kidneys are incised, the medulla appears dark red, and the cortex appears pale due to ischemia, with a striking contrast between the two.

　　(2) Microscopic examination: due to different etiologies, the pathological changes of acute renal failure are also different, and corresponding changes in renal blood vessels, glomeruli, renal tubules, and renal interstitium can appear. Acute tubular necrosis (ATN) can be divided into ischemic and toxic types. The lesions of toxic ATN are limited to the proximal tubules, showing focal distribution, with intact basal membranes of necrotic renal tubules and good regeneration of tubular epithelium. The lesions of ischemic ATN can involve all segments of renal tubules, showing diffuse distribution, with broken basal membranes of necrotic tubules and poor regeneration of epithelial cells.

　　2, Pathogenesis

　　The pathogenesis of acute renal failure is very complex, involving many factors and not fully elucidated. Different patients, with different etiology, condition, and course, have different pathogenesis. Currently, there are many theories about the pathogenesis of acute renal failure caused by renal ischemia and poisoning.

　　(1) The theory of acute tubular damage:

　　①The theory of tubular backflow: renal tubular lumen fluid leaks into the interstitium through broken tubular basement membranes, compressing capillaries, further reducing renal blood flow, leading to oliguria or anuria. It is now believed that backflow can also occur without tubular basement membrane breaks.

　　②The theory of tubular obstruction: tubular epithelial damage and swelling, various casts blocking, interstitial edema compressing, can all block the renal tubules, leading to oliguria or anuria.

　　③The vulnerability of the thick-walled ascending limb of the loop of Henle (mTAL) and the proximal straight tubule (S3): there is a delicate balance between oxygen supply and demand in the inner medulla, and the mTAL and S3 cells are in the marginal area of hypoxia. They are more susceptible to damage under ischemic and hypoxic conditions, and the further injury is exacerbated through ball-and-tube feedback, leading to ischemia of the renal parenchyma.

　　(2) The theory of renal hemodynamics change: due to the relatively mild pathological changes in the kidney tissue of ATN, the change in renal hemodynamics is an important mechanism for the occurrence of acute renal failure. These changes include:

　　①Rapid decrease in renal blood flow.

　　②The mechanism of glomerular arteriolar constriction:

　　A, activation of renin-angiotensin.

　　B, the effects of endothelin.

　　C, sympathetic nervous system activation.

　　D, the effects of prostaglandins (PGI2/TXA2 imbalance).

　　E, the effects of oxygen free radicals on endothelial cells.

　　F, others: catecholamines, antidiuretic hormone (ADH), platelet activating factor (PAF), etc.

　　③Swelling of glomerular capillary endothelial cells.

　　④Decreased glomerular ultrafiltration coefficient (kf).

　　⑤Vascular coagulation.

　　(3) Cellular mechanism:

　　①The way TP exhaustion occurs: through increasing intracellular free calcium; activating phospholipase A2; activating calpain; and inducing the disassembly of actin F, etc., which change the cytoskeleton, damage the cells, and ATP exhaustion is the central link in the pathogenesis of ATN.

　　The effects of vasoactive substances: mainly involve endothelin, NO, platelet activating factor (PAY), and renin-angiotensin-aldosterone system (RAS system), which have the overall effect of constricting renal blood vessels and damaging renal tubular epithelial cells.

　　③ Abnormal structure and function of renal tubules: Various factors lead to the destruction of the cytoskeleton, loss of cell polarity, destruction of the brush border of the proximal tubule, loss of tight junctions between cells and cell-matrix adhesion, and the destruction of the structure and function of renal tubules due to the formation of various casts and other factors.

　　④ The role of apoptosis: There are two apoptosis in ARF pathology, the first one appears immediately after renal injury, and the second one appears in the recovery period of ARF, playing an important role in the occurrence and recovery of ARF.

　　⑤ The role of growth factors: During ARF, the expression of immediate-early genes such as c-fos and egr-1 is upregulated, and the expression of epidermal growth factor EGF, IGF-1, FGF, HGF, and insulin-like growth factors is increased, mainly playing a role in cell regeneration and tissue repair.

　　Excess volume with concurrent congestive heart failure and pulmonary edema, arrhythmia, gastrointestinal bleeding due to gastritis or stress ulcer, convulsions, coma, and changes in behavior. Complications may also include pleural effusion, ascites, brain edema, hyperkalemia, hypocalcemia, hyponatremia, hypertension, and concurrent infection, etc.

　　1. Pulmonary edema refers to a condition caused by a disorder of the balance between the generation and return of pulmonary interstitial fluid due to certain reasons. A large amount of interstitial fluid cannot be absorbed by the pulmonary lymphatic and venous systems in a short period of time, leaking from the pulmonary capillaries, accumulating in the alveoli, interstitial tissue, and small bronchi, thus causing serious impairment of pulmonary ventilation and gas exchange function. Clinically, it is characterized by severe dyspnea, sitting breathing, cyanosis, profuse sweating, paroxysmal cough with a large amount of white or pink frothy sputum, symmetrical wet rales in both lungs, hazy shadow of butterfly shape in both lungs on X-ray chest film, shock and even death in the late stage, early arterial blood gas analysis may have low oxygen partial pressure, low carbon dioxide partial pressure, severe hypoxemia, carbon dioxide retention and mixed acidosis, which belongs to one of the clinical critical illnesses.

　　2. Congestive heart failure (CHF) refers to a pathological condition in which the cardiac output is insufficient to maintain tissue metabolism due to the dysfunction of cardiac contraction and/or relaxation, with an adequate return of venous blood.

　　3. Stress ulcer is an acute mucosal lesion of the stomach that occurs in severe stress responses such as multiple injuries, severe systemic infection, large-area burns, shock, and multi-organ failure. It is one of the common causes of upper gastrointestinal bleeding.

　　4. There is a potential space between the visceral and parietal layers of the pleura, known as the pleural cavity. Under normal circumstances, the width between the two pleural layers in the pleural cavity is about 10-20μm, containing serous fluid, about 0.1-0.2ml per kilogram of body weight, usually colorless and transparent, playing a lubricating role for the pleura. Its secretion and absorption are in a state of balance. Any factor causing an increase in secretion and/or a decrease in absorption will lead to the accumulation of fluid in the pleural cavity, forming pleural effusion.

　　5. Serum potassium level above 5.5mmol/L is called hyperkalemia, and >7.0mmol/L is considered severe hyperkalemia. Because hyperkalemia often has no or few symptoms and can suddenly lead to cardiac arrest, it should be detected and treated early.

　　6. Hyponatremia only indicates that the serum sodium ion concentration is below the normal level, which does not necessarily mean a true decrease in the body's sodium content. According to the urgency of onset, it can be divided into acute hyponatremia and chronic hyponatremia. The former refers to the decrease in serum sodium ion concentration below the normal level within 48 hours, otherwise it is chronic hyponatremia.

　　7. Normally, there is a small amount of fluid in the abdominal cavity of the human body (generally less than 200ml), which has a lubricating effect on intestinal peristalsis. Any pathological condition that causes an increase in the amount of fluid in the abdominal cavity, exceeding 200ml, is called ascites (ascites).

　　8. Without the use of antihypertensive drugs, systolic blood pressure ≥139mmHg and/or diastolic blood pressure ≥89mmHg, hypertension is divided into stages 1, 2, and 3 according to blood pressure levels. Systolic blood pressure ≥140mmHg and diastolic blood pressure

　　First, oliguria type acute renal insufficiency

　　It can be divided into oliguria phase, diuresis phase, and recovery phase, and the boundaries between the periods in children are often not clear.

　　1. Oliguria phase

　　ARF, especially acute tubular necrosis, often has a significant oliguria phase, lasting about 10-14 days.

　　(1) Oliguria: In the neonatal period, urine output <1ml/(kg·h), in infants <200ml/d, in the pre-school period <300ml/d, and in the school age period <400ml/d is considered oliguria; if <50ml/d, it is considered anuria.

　　(2) Azotemia: Increased blood BUN and Cr, and systemic symptoms of intoxication caused by the retention of toxins in the body, such as anorexia, nausea, vomiting, hematemesis, drowsiness, irritability, anemia, and so on.

　　(3) Water and sodium retention: Generalized edema, increased blood pressure, and may also appear with pulmonary edema, cerebral edema, heart failure, and other manifestations.

　　(4) Electrolyte disorder: Hyperkalemia, which may manifest as irritability, nausea, vomiting, drowsiness, numbness of the limbs, chest tightness, shortness of breath, slow heart rate, irregular heartbeat, ECG showing tall T waves, widened QRS complexes, etc.; hyponatremia, which may cause apathy, poor response, nausea and vomiting, even convulsions, etc.; hyperphosphatemia and hypocalcemia, which may cause tetany of the hands and feet, convulsions, and so on.

　　(5) Metabolic acidosis: Manifested as fatigue, drowsiness, flushed face, nausea, vomiting, deep breathing, even coma, shock, and so on.

　　(6) Endocrine and metabolic changes: Increased PTH, decreased calcitonin (CT); decreased T3, T4, normal TSH; decreased erythropoietin; increased ADH and renin-angiotensin-aldosterone activity; increased growth hormone; decreased glucose tolerance and insulin resistance, increased insulin and glucagon levels.

　　2. Diuretic phase

　　When urine output exceeds 2500ml/m2, it enters the polyuria phase. Kidney function gradually recovers, and blood BUN and Cr decrease several days after the onset of polyuria. The symptoms of systemic toxicity caused by toxic accumulation are alleviated. Dehydration and hypokalemia, hyponatremia are prone to occur during the polyuria phase.

　　3. Recovery period

　　After the polyuria phase, urine output gradually returns to normal, blood BUN and Cr gradually normalize, and the tubular concentrating function and acidifying function of the kidneys also gradually recover. A few may have varying degrees of renal function damage, manifested as chronic renal insufficiency, requiring dialysis treatment to be maintained.

　　Second, non-oliguric acute renal insufficiency

　　1. There is no oliguria, with an average daily urine output of more than 1000ml.

　　2. Often secondary to kidney damage caused by aminoglycoside antibiotics and contrast agents.

　　3. Clinical manifestations are less common in oliguria, with fewer complications and a lower mortality rate.

　　Third, hypermetabolic acute renal insufficiency

　　1. Etiology

　　It often occurs secondary to large-area burns, crush injuries, major surgeries, and severe infections, sepsis.

　　2. Changes in blood biochemistry

　　Organ catabolism is extremely vigorous, with blood BUN, Cr, and blood potassium rapidly rising, and HCO3- rapidly falling. Blood BUN increases by more than 14.3 mmol/L per day, blood Cr increases by more than 176 μmol/L per day, and blood K increases by more than 1.0 mmol/L per day.

　　3. High mortality rate

　　Hyperkalemia and metabolic acidosis are extremely serious with a high mortality rate.

　　Firstly, there must be a reasonable protein intake. The main source of metabolic products in the human body is the protein components in the diet, therefore, in order to reduce the workload of the remaining kidney, the protein intake must be adapted to the kidney's excretion capacity.

　　1. B-ultrasound examination

　　It can observe kidney size and also suggest the presence of kidney stones and hydronephrosis. If the examination shows normal kidney size but significant hydronephrosis, it strongly suggests a post-renal etiology.

　　2. Abdominal X-ray film

　　Used to observe kidney size and can also detect positive stones.

　　3. Blood routine

　　Commonly, there is a mild decrease in hemoglobin and red blood cells. In cases of secondary infection, there is often an increase in white blood cells and left shift of the nucleus, and some individuals may have a decrease in platelets.

　　4. Blood biochemistry

　　The changes during oliguria are most significant, with significant increases in blood urea nitrogen and creatinine, a marked decrease in bicarbonate, and the occurrence of various electrolyte imbalances, with hyperkalemia and hyponatremia being most common. Low calcium and high phosphorus can also occur. In the early stage of polyuria, there is often significant metabolic acidosis and azotemia, and blood electrolytes often show abnormalities, especially prone to hypokalemia or hypernatremia.

　　5. Urinalysis

　　Common symptoms include reduced urine specific gravity and proteinuria, with red blood cells, white blood cells, and casts visible in the sediment under a microscope. If caused by pre-renal factors, the urine specific gravity is often elevated in the early stage, and no abnormalities are usually found in urine sediment microscopy and urine protein quantification. If caused by renal factors, there is often significant proteinuria and abnormalities in urine sediment microscopy.

　　6. Renal biopsy

　　The indications are acute renal failure caused by renal causes, which can understand the pathological type and degree of renal lesions, and help to formulate treatment plans and judge the prognosis.

　　7. Radionuclide examination (SPECT)

　　It helps to identify renal vascular lesions (embolism) caused by ARF and post-renal ARF caused by obstruction; when there is tubular necrosis, the 99mTc diethylenetriamine pentaacetic acid (DTPA) three-phase dynamic imaging shows good perfusion and poor absorption, while 131I-iodomethacetate (OIH) shows unclear renal imaging, with certain specificity.

　　1. Calorie

　　Choose sugar as the main source of calories, and provide appropriate amounts of fat, high-quality protein, and minerals and vitamins

　　2. Protein

　　Choose high-quality protein, and adjust the amount according to the renal function status and the situation during the treatment process. In the case of acute renal insufficiency, the amount should not exceed 30g/day.

　　3. Electrolytes and vitamins

　　The intake of sodium should be determined according to the patient's renal retention and excretion capacity of sodium, as well as whether there is hypertension, heart failure, edema, and other conditions, and the intake of vitamins should be increased.

　　1. Treatment

　　In addition to the treatment of the cause, the main treatment is to help the child survive the renal failure period, minimize the internal environment disorder caused by oliguria, and strive for the recovery of renal lesions.

　　1. Maintain the balance of water and electrolytes

　　When conducting a physical examination, it is necessary to estimate the child's fluid status, and it is sometimes difficult to distinguish between oliguria caused by insufficient blood volume and acute tubular necrosis. When there is insufficient blood volume, urine is concentrated (urine osmolality is higher than 500mmol/L, urine sodium is often lower than 20mmol/L), and the urine sodium fraction is often less than 1%. When there is tubular necrosis, urine is diluted (urine osmolality is approximately 350mmol/L, urine sodium is often higher than 40mmol/L), and the urine sodium fraction is often higher than 1%.

　　If there is a decrease in blood volume without bleeding and without hypoalbuminemia, colloid expansion is not needed. Intravenous injection of isotonic saline 20ml/kg is sufficient within 30 minutes, and the patient will urinate more than 2 hours later. If the child still does not urinate, a catheter should be inserted to measure the bladder urine volume and central venous pressure. If clinical and laboratory examinations indicate that the body fluids have been replenished, diuretics should be considered. Although diuretics are ineffective for children with anuria, they cannot change renal function nor affect the natural process of renal failure, but these drugs such as furosemide or mannitol act on the change of renal tubular function, accelerate urine flow, and are valuable for the treatment of hyperkalemia and body fluid retention in some oliguric patients due to promoting urine excretion. The intravenous dose of furosemide is 2mg/kg, and the speed is 4mg/min; if there is no response, the second dose of 10mg/kg can be given, and if the urine output does not increase, furosemide can be trusted, and mannitol 0.5g/kg can be given intravenously once, regardless of whether there is a response, to avoid toxic reactions, mannitol should not be used again. If the patient has no hypertension, dopamine can be used in combination, 5μg/(kg·min), to increase renal cortical blood flow with diuretics.

　　If there is still no adequate urine output after sufficient blood volume is replenished or diuretics are administered, the intake of fluid should be strictly limited. The amount of fluid restriction should be determined according to the fluid status, if the patient has oliguria or anuria while the blood volume is normal, the fluid intake should be limited to the amount of insensible water loss [400ml/(m2·24h) or 1ml/(kg·h)] plus the urine output on that day. If there is fluid retention in the body, the intake of fluid should be completely restricted to reduce the expanded blood volume. Generally, a 10% to 30% glucose solution without electrolytes is used to maintain vascular volume through the slowest infusion pump, and the infusion content can also be improved according to the electrolyte balance. In addition to excessive fluid retention in the body, renal extrarenal fluid loss such as bleeding, abnormal gastrointestinal loss (vomiting, diarrhea) should be supplemented.

　　2. Treatment of hyperkalemia

　　Acute renal failure can rapidly lead to hyperkalemia (blood potassium level above 6mmol/L), which can cause arrhythmias and death. The earliest ECG change in patients with hyperkalemia is a peak-shaped T wave, followed by a decrease in the ST segment, prolongation of the PR interval, widening of the QRS interval, ventricular fibrillation, and cardiac arrest. When the serum potassium level reaches 5.5mmol/L, the patient's fluid should contain a high concentration of glucose, and 1g/kg of potassium-lowering resin should be administered orally or by retention enema. Potassium-lowering resin is a medicinal sodium exchange resin that, when taken orally or enema, can produce ion exchange in the intestines, absorb potassium, and excrete it out of the body with feces, thereby lowering blood potassium levels. The advantage of sodium resin is that it will not exacerbate intoxication and also absorbs ammonium ions in the intestines of uremic patients, which can reduce the synthesis of urea. It is best to take the potassium-lowering resin added to 2ml/kg of 70% sorbitol as a suspension, as sorbitol can cause osmotic diarrhea, which can cause the loss of water and electrolytes (uremic patients often have fluid retention, and the levels of sodium and potassium in the body are both increased), thus promoting the excretion of water and electrolytes through the gastrointestinal tract. 70% sorbitol can cause local irritation to the rectum when used for enema, and it is recommended to use a 20% concentration while the dose can be increased to 10mg/kg. Resin treatment can be repeated every 2 hours, and attention should be paid not to cause sodium overload.

　　If the serum potassium level rises to 7mmol/L or more, in addition to using potassium-lowering resins, the following treatments should be added.

　　(1) Intravenous injection of 0.5mg/kg of 10% calcium gluconate should be slowly infused, and heart rate should be closely monitored. If the heart rate decreases by 20 times per minute, the infusion should be stopped until the heart rate returns to the speed before infusion.

　　(2) Intravenous injection of 3mmol/kg of 5% sodium bicarbonate should be avoided to prevent volume expansion, hypertension, and convulsions.

　　(3) The mixture of 50% glucose 1mg/kg and insulin (1U insulin requires the supply of 5g of glucose) should be injected intravenously for more than one hour, and close monitoring is required to prevent hypoglycemia.

　　Calcium gluconate does not reduce serum potassium levels, but can antagonize the myocardial irritability caused by potassium. The mechanism by which sodium bicarbonate reduces blood potassium levels is not yet clear. The mixture of glucose and insulin injected intravenously is used to transfer extracellular potassium into the cells. A spray of β-adrenergic receptor agonists can also quickly reduce blood potassium levels. The above emergency treatment only takes a few hours, if hyperkalemia persists and does not decrease, dialysis treatment must be performed.

　　3. Correcting acidosis

　　In renal failure, there is often moderate acidosis due to insufficient excretion of hydrogen and ammonium ions, and it is rare that treatment is needed. Severe acidosis (arterial pH < 7.15, serum bicarbonate < 8mmol/L) can increase the irritability of the myocardium, so it must be treated. Due to the danger of rapid infusion of alkaline solution, only partial acidosis needs to be corrected intravenously, and carbonic acid salt is given to raise the arterial pH to pH 7.2 (approximately serum sulfate hydrogen salt 12mmol/L), the correction formula is as follows:

　　The requirement for NaHCO3 (mmol) = 0.3 × body weight (kg) × [12 - serum bicarbonate (mmol/L)].

　　After the serum calcium and phosphorus reach normal values, bicarbonate sodium or sodium citrate solution can be taken orally to correct acidosis.

　　In renal failure, hyperphosphatemia and corresponding hypocalcemia occur due to impaired excretion of phosphorus, but since there is acidosis at the same time, the concentration of free calcium in the blood usually does not decrease, so convulsions do not occur; if acidosis is corrected rapidly, the concentration of free calcium will decrease and convulsions may occur.

　　4. Hypocalcemia

　　The method of reducing serum phosphorus can be used, except for children with tetany, calcium can be supplemented without intravenous administration. Generally, calcium carbonate antacids combined with phosphates can be taken orally to increase the excretion of phosphates in the feces.

　　5. Hyponatremia

　　Hyponatremia is often corrected by oliguria or anuria. If the serum sodium level is below 120mmol/L, the risk of cerebral edema and intracranial hemorrhage increases. If the patient does not have dehydration, the intake should be restricted. If the serum sodium level falls below 120mmol/L, then high concentration (3%) sodium chloride should be infused intravenously to raise the serum sodium level to 125mmol/L. The calculation formula is as follows: NaCl requirement (mmol) = 0.6 body weight (kg) × [125 - serum sodium (mmol/L)]. The risk of administering hypertonic saline includes expansion of body fluids, hypertension, and congestive heart failure. If the above conditions occur, dialysis therapy should be considered.

　　6. Gastrointestinal bleeding

　　Calcium carbonate antacids can be used to prevent the occurrence of hypertension, and can also reduce serum phosphorus. Metoclopramide (cimetidine) 5 to 10mg/(kg·12h) can also be administered intravenously.

　　7. Hypertension

　　The condition can be due to the primary disease, expansion of extracellular fluid, or both. For patients with renal failure and hypertension, it is very important to restrict salt and water intake. For children with severe hypertension, diazoxide (chlorphenothiazide, diazoxide) can be used, 5mg/kg (single maximum dose 300mg) is injected intravenously within 10 seconds, and blood pressure can usually drop within 10 to 20 minutes. If the effect is not satisfactory, the drug can be repeated after 30 minutes after the first injection, or nifedipine (nifedipine 0.25 to 0.5mg/kg, sublingual administration) can be used quickly. For hypertensive emergencies, sodium bicarbonate or labetalol (labetolol) can be continuously infused intravenously, while for patients with less severe hypertension, the expansion of extracellular fluid volume can be controlled (by restricting salt and water intake, using furosemide), and β-adrenergic receptor blockers such as propranolol and vasodilators are often effective.

　　8. Other

　　Convulsions may be related to the primary disease, such as systemic lupus erythematosus, hyponatremia (water intoxication), hypocalcemia, hypertension, or due to uremia itself. Treatment should be aimed at the primary disease. Anticonvulsant drugs such as chloral hydrate, phenobarbital, and phenytoin are ineffective in uremic patients. Diazepam is effective in controlling convulsions.

　　Except for hemolysis (such as hemolytic uremic syndrome, lupus) or bleeding, anemia in general acute renal failure is mild (hemoglobin 90-100g/L) due to fluid expansion and does not require blood transfusion. If there is acute bleeding, hemolytic anemia, or persistent renal failure, and hemoglobin drops to 70g/L, blood transfusion is required. Blood transfusion in patients with fluid overload can lead to fluid expansion, resulting in hypertension, congestive heart failure, and pulmonary edema. Slowly (4-6 hours) transfusing fresh blood (reducing potassium intake) can reduce fluid expansion by 10ml/kg. If there is severe fluid retention, it is necessary to correct anemia during dialysis.

　　Most children who were originally healthy or well-nourished may only consume fat and carbohydrate diets at first when suddenly developing acute renal failure, and need to limit sodium, potassium, and water intake. If renal failure persists for about 7 days, consider oral intake and parenteral administration of essential amino acids.

　　The indications for acute renal failure dialysis therapy include the combination of the following factors: acidosis, electrolyte imbalance, especially hyperkalemia, central nervous system disturbance, hypertension, fluid retention, and congestive heart failure. If dialysis treatment is started in time for children with acute renal failure, it can significantly improve the survival rate of children.

　　Some patients with acute renal failure may reduce complications and delay dialysis treatment by using conservative treatment cautiously; some may still need dialysis therapy. The life-threatening complications of uremia include bleeding, pericarditis, and central nervous system dysfunction.

　　II. Prognosis

　　The prognosis varies depending on the cause. Prerenal renal failure can usually be recovered with proper treatment. Among children with renal renal failure, acute glomerulonephritis has the best prognosis. The prognosis of non-oliguric acute renal failure is better with less urine or anuria; the younger the age, the worse the prognosis, especially those with urinary system malformations or congenital heart disease; among school-age children, the prognosis of rapidly progressive glomerulonephritis is the worst.