Acute glomerulonephritis in children

　　Although pediatric acute glomerulonephritis has various etiologies, the vast majority of cases are immune complex glomerulonephritis caused by acute infection with Group A beta-hemolytic streptococcus. The incidence of nephritis after streptococcal infection is generally 0% to 20%.

　　In addition to Group A beta-hemolytic streptococcus, other bacteria such as viridans streptococcus, pneumococcus, Staphylococcus aureus, Salmonella typhi, Haemophilus influenzae, and viruses such as Coxsackievirus, ECHO virus type 9, measles virus, mumps virus, hepatitis B virus, cytomegalovirus, Epstein-Barr virus, influenza virus, as well as parasites such as Plasmodium, Mycoplasma pneumoniae, Candida albicans filaments, hookworm, schistosoma, toxoplasma, Treponema pallidum, and Leptospira can also cause acute glomerulonephritis.

　　The complications of pediatric acute glomerulonephritis are mainly complications during the acute phase. The severe complications during the acute phase mainly include severe circulatory congestion, hypertensive encephalopathy, and acute renal failure.

　　1. Severe circulatory congestion: High water and sodium retention can cause severe circulatory congestion, heart failure, and edema. Manifestations include marked edema, persistent oliguria, or anuria, palpitations, shortness of breath, irritability, inability to lie flat, cyanosis, rales in both lungs, dull heart sounds, increased heart rate, gallops, and progressive enlargement of the liver.

　　2. Hypertensive encephalopathy: Refers to the symptoms of central nervous system involvement due to a sharp increase in blood pressure (especially diastolic pressure). It often occurs in the early stage of acute glomerulonephritis, with an acute onset, manifested by severe headache, frequent nausea and vomiting, followed by visual disturbances, dizziness, diplopia, transient blindness, and symptoms such as drowsiness or irritability. If not treated promptly, it can lead to seizures, coma, and in a few cases, transient hemiparesis and aphasia. Severe cases can lead to cerebral hernia. A diagnosis can be made if blood pressure exceeds 18.7/12.0 kPa (140/90 mmHg) and is accompanied by one of the following: visual disturbances, seizures, or coma.

　　3. Acute renal failure: Only a very small number of cases progress to acute renal failure. Clinical manifestations include oliguria or anuria, increased blood urea nitrogen and serum creatinine, hyperkalemia, and metabolic acidosis.

　　The clinical manifestations of pediatric acute glomerulonephritis vary greatly in severity, with mild cases showing no clinical symptoms and only microscopic hematuria detected, while severe cases can present an acute progressive course with renal insufficiency developing in a short period of time.

　　1. Preceding Infection

　　90% of the cases have a preceding streptococcal infection, mainly involving respiratory and skin infections. After the preceding infection, the disease starts acutely after a symptom-free interval of 1 to 3 weeks. Pharyngitis as a trigger usually presents with fever, enlarged cervical lymph nodes, and pharyngeal secretion 6 to 12 days before the onset of the disease (on average, 10 days). Skin infections are usually seen 14 to 28 days before the onset of the disease (on average, 20 days).

　　Two, typical manifestations

　　During the acute phase, there are often general malaise, fatigue, loss of appetite, fever, headache, dizziness, cough, dyspnea, nausea, vomiting, abdominal pain, and epistaxis, etc.

　　1. Edema 70% of cases have edema, generally only involving the eyelids and facial area, while severe cases may spread to the whole body within 2 to 3 days, presenting as non-pitting edema.

　　2. Hematuria 50% to 70% of patients have gross hematuria, which persists for 1 to 2 weeks and then changes to microscopic hematuria.

　　3. The degree of proteinuria varies. 20% may reach nephrotic level. Pathologically, proteinuria patients often show severe mesangial proliferation.

　　4. Hypertension 30% to 80% of cases have increased blood pressure.

　　5. Reduced urine output and severe gross hematuria may be accompanied by difficulty in urination.

　　Three, severe manifestations

　　A few children may appear the following severe symptoms in the early stage of the disease (within 2 weeks):

　　1. Severe circulatory congestion often occurs within one week of onset, due to water and sodium retention, resulting in increased plasma volume and circulatory congestion. When nephritis children show tachypnea and wet rales in the lungs, the possibility of circulatory congestion should be alert. Severe cases may have difficulty breathing, orthopnea, jugular vein distension, frequent coughing, expectoration of pink frothy sputum, widespread wet rales in both lungs, cardiac enlargement, and even gallops, liver enlargement and hardness, and exacerbation of edema. A few cases may suddenly occur, with an acute deterioration in the condition.

　　2. Hypertensive encephalopathy is caused by cerebral vasospasm, leading to ischemia, hypoxia, and increased vascular permeability, resulting in cerebral edema. In recent years, some people believe it is caused by cerebral vasodilation. It often occurs in the early stage of the disease, after a sudden increase in blood pressure, and the blood pressure is often above 150-160/100-110 mmHg. Older children may complain of severe headache, vomiting, diplopia, or transient blindness. Severe cases may suddenly develop seizures and coma.

　　3. Acute renal insufficiency often occurs in the early stage of the disease, with symptoms such as oliguria and anuria, causing transient azotemia, electrolyte disturbance, and metabolic acidosis, which usually lasts for 3 to 5 days, not exceeding 10 days.

　　Four, atypical manifestations

　　1. Asymptomatic acute nephritis is a subclinical case, where the child only has microscopic hematuria or only a decrease in serum C3 without other clinical manifestations.

　　2. Extra-renal symptomatic acute nephritis Some children have significant edema and hypertension, even severe circulatory congestion and hypertensive encephalopathy. At this time, the urine changes are slight or the urinalysis is normal, but there is a pre-streptococcal infection and a significant decrease in blood C3 level.

　　3. Acute nephritis with nephrotic syndrome manifestation A few children with acute nephritis may present with acute nephritis, but with prominent edema and proteinuria, accompanied by mild hypercholesterolemia and hypoalbuminemia, with clinical manifestations similar to nephrotic syndrome.

　　The fundamental prevention of acute glomerulonephritis in children is the prevention and treatment of streptococcal infection. In daily life, it is necessary to strengthen physical exercise and pay attention to skin cleanliness and hygiene to reduce respiratory and skin infections. If infection occurs, it should be treated promptly and thoroughly. Urinalysis should be performed 2 to 3 weeks after infection to detect any abnormalities in time. Sufficient rest is required, and bed rest should be maintained until the edema significantly subsides, blood pressure returns to normal, and gross hematuria disappears, which usually takes 2 to 3 weeks. School attendance can resume after the sedimentation rate returns to normal, but the amount of activity should be controlled.

　　Typical acute nephritis is not difficult to diagnose. For those with difficult clinical diagnosis, renal biopsy is necessary for diagnosis in case.

　　One, Urinalysis

　　Urine changes have a great individual difference, generally manifested as:

　　1. Urine output is low and the specific gravity is high.

　　2. Gross hematuria is common, with the urine appearing as a smoky coffee color, often accompanied by red blood cell casts, and the red blood cells in the urine sediment are deformed.

　　3. Proteinuria is common, but the degree varies. Generally, the 24-hour urine protein excretion is 0.2 to 3.0g. If proteinuria is marked and persists for a long time, nephrotic syndrome may occur.

　　4. White blood cells and white blood cell casts are present in the urine, especially significant in the early stage.

　　5. Various types of casts in urine: in addition to red blood cell casts and white blood cell casts, there can also be hyaline casts, granular casts, and hyaline casts, etc.

　　Two, Blood Examination

　　1. Red blood cell count and hemoglobin can be slightly low, which is due to: ① expansion of blood volume, dilution of blood, ② decrease in erythropoietin in patients with renal failure leading to renal anemia, ③ hemolytic anemia.

　　2. White blood cell count can be normal or increased, which is related to whether the primary infection focus continues to exist.

　　3. Erythrocyte sedimentation rate (ESR) usually increases, and it can return to normal within 1 to 3 months.

　　Three, Blood Biochemistry and Renal Function Tests

　　Glomerular filtration rate (GFR) shows a decrease of varying degrees, but renal plasma flow can still be normal, so the filtration fraction is often reduced. Compared with glomerular dysfunction, renal tubular function is relatively good, and renal concentrating function can usually be maintained. Clinically, transient azotemia is common, with mild elevation of blood urea nitrogen and creatinine. In cases with acute renal insufficiency, marked elevation of blood urea nitrogen and creatinine may occur. Depletive hyponatremia can occur in children who do not limit fluid intake. In addition, children may have hyperkalemia and metabolic acidosis. Plasma protein may slightly decrease due to blood dilution. In patients with urinary protein levels reaching nephrotic syndrome, serum albumin levels decrease significantly, and may be accompanied by a certain degree of hyperlipidemia.

　　Evidence of Streptococcal Infection

　　Skin lesion or throat swab bacterial culture can be performed to detect Group A beta-hemolytic Streptococcus, or to check for antibodies against streptolysin or enzymes in the serum, with elevated anti-O (ASO) seen in more than 80% of patients with respiratory tract infections as prodromal symptoms and 50% of patients with impetigo as prodromal symptoms. Generally, the level begins to rise 2 to 3 weeks after infection, reaching a peak in 3 to 5 weeks, and returns to normal within half a year. Anti-deoxyribonuclease B (anti-DNAaseB), anti-hyaluronidase (anti-Htase), and anti-diphosphopyridine nucleotidease (anti-ADPNase) can also be detected, and the increase in these enzyme activities are evidence of streptococcal infection. Anti-Htasc has a higher positive rate in skin infections, while Anti-ADPNase has a higher positive rate in respiratory tract infections, and Anti-ADPNaseB has a positive rate >90% in both infections.

　　Five, Immunological examination

　　The decrease in the level of serum total complement (CH50) and complement 3 (C3) is a key to diagnosing acute glomerulonephritis, but the degree of decrease is not related to the extent of the lesion and the prognosis; the levels of serum gamma globulin and immunoglobulin IgG are often increased; the level of serum complement 4 (C4) is normal or slightly decreased, and the decreased serum complement 3 usually returns to normal within 1 to 2 months, but a few may take 3 months to return to normal.

　　Six, Renal biopsy

　　Early manifestations are capillary infiltration and proliferative inflammation, with proliferation of endothelial cells and mesangial cells, and a large amount of sedimentation under the epithelium, presenting in the shape of a camel's hump. In the later stage, mild mesangial proliferation is the main feature, and severe patients may appear a large number of crescent bodies.

　　Seven,Electrocardiogram.

　　It can be manifested as low voltage, low T-waves, and other changes.

　　Eight, X-ray

　　The chest X-ray may show a slight increase in the cardiac shadow; when severe circulatory congestion occurs, signs of pulmonary edema may be found.

　　Nine, Ultrasound examination

　　The kidneys appear normal or diffusely enlarged, with enhanced cortical echo; when severe circulatory congestion occurs, the liver may increase in size.

　　Low-salt diet is also one of the main measures for treating acute glomerulonephritis in children. It is recommended to consume easily digestible and nutritious foods, avoid spicy and刺激性 foods as well as greasy and fatty foods, and eating fresh vegetables and fruits is beneficial for recovery.

　　It is recommended to use a variety of staple foods, such as corn flour and high-strength flour to make steamed cakes or dumplings with rice porridge. The dietary requirements for vegetables and fruits for patients with acute glomerulonephritis are rich in vitamins, low in potassium and sodium. Vegetables can be chosen from vegetables such as rapeseed, onions, and tomatoes, and fruits can include apples, strawberries, grapes, and oranges. The selection of protein generally focuses on high-quality animal proteins such as milk, eggs, hairtail, and beef, but it should be limited and not consumed excessively.

　　The immune pathogenesis of nephritis involves multiple links, such as the formation of antigens, antibodies, immune complexes, and the participation of various mediators, therefore, the treatment of nephritis should aim to eliminate or weaken these links. Some treatment measures currently used in clinical practice have achieved good efficacy, such as the use of adrenal cortical hormones and cyclophosphamide in the treatment of minimal change nephrotic syndrome, and some may be effective; anticoagulation therapy is used for some glomerular diseases; further in-depth research is still needed to find effective treatment methods.

　　The main treatment for pediatric acute glomerulonephritis is to clear residual pathogens in the body, to treat symptoms, protect renal function, and prevent complications.

　　One. General treatment

　　1. Rest: Regardless of the severity of the condition, bed rest should be maintained in the early stage until significant edema subsides, blood pressure returns to normal, and gross hematuria disappears. This usually takes 2 to 3 weeks. School can be attended after the erythrocyte sedimentation rate returns to normal, but physical activity should be controlled before the urine Addis count returns to normal.

　　2. Diet: During the acute phase, water, salt, and protein intake should be restricted. Generally, low-salt or salt-free, low-protein diets are adopted, using sugar to provide calories. Salt intake should be controlled at 1 to 2 g/d. For those with renal insufficiency, high-quality protein should be used, with an intake of 0.5 g/(kg·d) as appropriate. For those with severe edema and oliguria, water intake should be restricted.

　　Two. Antibiotics The main purpose is to clear residual pathogens, and penicillin 200,000 to 300,000 U/(kg·d) or erythromycin 30 mg/(kg·d) can be administered intravenously for 2 weeks. If other pathogens are suspected, other antibiotics can be added. Erythromycin can be used for those allergic to penicillin.

　　Three. Symptomatic treatment includes diuresis, edema reduction, and antihypertension.

　　1. Diuretics: For mild edema, hydrochlorothiazide (hydrochlorothiazide, DHCT) 2 to 3 mg/(kg·d) can be taken orally. After an increase in urine output, spironolactone (spironolactone, antisterone) 2 mg/(kg·d) can be added orally. For patients with poor response to oral diuretics or severe edema, intravenous or intramuscular furosemide (furosemide,速尿) can be administered, 1 to 2 mg/kg per dose. New-generation diuretic combinations, such as dopamine and phentolamine at 0.3 to 0.5 mg/kg and furosemide 2 mg/kg, can also be used together with 10% glucose 100 to 200 ml for intravenous infusion, which has better diuretic effects than furosemide alone.

　　2. Antihypertensive: Nifedipine (nifedipine,心痛定) is the first choice, 0.25 to 0.5 mg/kg per dose, taken orally or sublingually 3 to 4 times a day. If blood pressure cannot be controlled, nicardipine (nieardipine, 佩尔地平, perdipine) 0.5 to 1 mg/kg per dose, twice a day; captopril (captopril,巯甲丙脯氨酸) 1 to 2 mg/(kg·d), 2 to 3 times a day; prazosin (prazosin) 0.02 to 0.05 mg/kg per dose, taken orally 3 to 4 times a day.

　　Four. Treatment for severe cases

　　1. Acute renal insufficiency: Patients with acute glomerulonephritis may experience a decrease in urine output during the first 1 to 2 weeks of onset, with possible azotemia. As the renal lesions improve, urine output increases, and BUN, Cr also decrease to normal levels. However, a few children may have severe lesions, with thrombosis in the glomerular capillaries,纤维素-like necrosis, or hyperplasia of epithelial cells, with fibrin deposition, forming large areas of crescent bodies quickly, which can lead to severe oliguria or anuria, renal failure, and may also develop into rapidly progressive nephritis.

　　(1) oliguria phase: Maintain electrolyte and acid-base balance, and strengthen diuresis.

　　A, Strict control of water intake: 'Output equals input', only supplementing insensible water loss at a rate of 400ml/(m2·d) or [infants 20ml/(kg·d), children 15ml/(kg·d), adolescents 10ml/(kg·d)] and the urine output and abnormal loss of the previous day.

　　Daily fluid volume = urine output + insensible water loss - endogenous water produced by food metabolism and tissue breakdown.

　　For every 1℃ increase in body temperature, increase water intake by 75ml/(m2·d), supplementing insensible water loss with sodium-free liquids. Peripheral infusion can use 10% to 20% glucose, and central venous infusion can use 30% to 50% glucose. Endogenous water is 100ml/(m2·d). Abnormal losses, including vomiting, diarrhea, and gastrointestinal drainage, should be supplemented with 1/4 to 1/2 of the fluid.

　　Every day, the water status of the patient should be assessed, including clinical signs of dehydration or edema; weight should be measured every day. If the intake control is appropriate, the weight should decrease by 10 to 20mg/kg per day, blood sodium should not be below 130mmol/L, and blood pressure should be stable.

　　B, Caloric and protein intake: Provide sufficient calories to reduce protein breakdown. In the early stage, only carbohydrates should be given, with glucose supplied at 3 to 5mg/(kg·d) intravenously. This can reduce the body's own protein breakdown and ketone body production. When the condition improves and oral intake is possible, basic metabolic calories [children 30kcal/(kg·d), infants 50kcal/(kg·d)] should be given as soon as possible. The diet can include low-protein, low-sodium, low-potassium, and low-phosphorus foods. Protein should be limited to 0.5 to 1.0mg/(kg·d) and should be of high quality, such as egg, meat, and dairy protein. To promote protein synthesis, nandrolone phenylpropionate 25mg can be administered intramuscularly 1 to 2 times a week. For those with a high catabolic state or unable to take oral intake, intravenous hyperalimentation can be considered.

　　C, Treatment of hyperkalemia: Blood potassium levels greater than 6.5mmol/L are a dangerous threshold, and active treatment should be implemented. If there are significant EKG changes, 0.5 to 1ml/kg of 10% calcium gluconate can be administered intravenously slowly over 15 to 30 minutes; or 3 to 5ml/kg of 5% NaHCO3 can be administered intravenously, or 20% glucose (0.5g/kg) mixed with insulin (0.2U/g glucose) can be infused over 2 hours. If the above treatments are ineffective or blood potassium levels remain above 6.5mmol/L, dialysis treatment should be considered.

　　a, Bicarbonate: It can correct acidosis, form mild alkalosis in extracellular fluid, and transfer potassium from extracellular to intracellular spaces, while also expanding the extracellular volume, diluting the blood potassium concentration. It can be administered with 2ml/kg of 5% sodium bicarbonate intravenously within 5 minutes. If the condition has not returned to normal, it can be repeated after 15 minutes. Sodium solution acts quickly but has a short duration, only maintaining for 30 to 90 minutes.

　　b, Calcium Gluconate: Calcium can counteract the toxicity of potassium to the myocardium. 10% calcium gluconate 10ml is administered intravenously, and it starts to take effect within 5 minutes, lasting for 1 to 2 minutes. It can be used 2 to 3 times a day, but those using digitalis should use it with caution.

　　C, Hypertonic glucose and insulin: Promote potassium into the cell, 1U insulin for every 3-4mg of glucose. 1.5mg/kg of glucose can temporarily reduce blood potassium by 1-2mmol/L, starting to take effect within 15 minutes, and lasting for 12 hours or longer. It can be repeated if necessary.

　　The above three therapies can be used alone or in combination during emergency treatment for hyperkalemia, and they have certain efficacy. However, they cannot be sustained, so dialysis should be prepared during treatment.

　　Cation exchange resin: After the above resuscitation, EKG tends to return to normal, but blood potassium is still between 5.5-7mmol/L. Cation exchange resin can be administered orally or enema at a dose of 0.3-1mg/(kg·time). This drug is prone to cause constipation, and it can be mixed with 10%-20% sorbitol for oral or enema administration. Sorbitol has osmotic diarrhea effects, and it starts to take effect within 30-60 minutes after enema. It can be repeated 2-4 times a day, or it can be taken orally in capsules. For every 1mmol of potassium absorbed by the cation resin, 1mmol of other cations, such as sodium, are released. Attention should be paid to sodium retention if sodium is considered.

　　Dialysis: Both hemodialysis and peritoneal dialysis are effective. The former has a faster effect, and blood potassium can be reduced from 7.5-8mmol/L to normal range within 1-2 hours, while peritoneal dialysis requires 4-6 hours to reach normal.

　　To prevent and treat hyperkalemia, it is necessary to reduce the body's high protein catabolic metabolism, provide sufficient calories, limit high-potassium diet and medications, and avoid transfusing stored blood, etc.

　　Hyponatremia: It should be distinguished whether it is dilutional or hyponatremic. During the oliguria period, the former is more common. The intake of water should be strictly controlled, diuresis, and it can usually be corrected. Generally, it is not necessary to correct it with hypertonic saline, as this may cause excessive volume and lead to heart failure. In hyponatremic patients, when blood sodium

　　Metabolic acidosis: Mild cases often do not require treatment. When blood HCO3-

　　Hypertension, heart failure, and pulmonary edema: Often related to excessive blood volume and water intoxication. Treatment should strictly limit the intake of water, salt restriction, and diuresis. Diuretics can use furosemide 2-3mg/(kg·time), 2-3 times a day. In case of hypertensive encephalopathy, sodium nitroprusside can be administered intravenously. Sodium nitroprusside 10-20mg can be added to 100ml of 5% glucose solution, and the infusion rate can be adjusted from 1-8?g/(kg·min) according to blood pressure to stabilize blood pressure at a certain level. Vasodilation can be achieved by adding dopamine and phenylephrine each 10mg to 100ml of 10% glucose solution for intravenous infusion, once a day, for 7 consecutive days. The combination of the two drugs can dilate renal arteries and improve renal blood flow.

　　Treatment of heart failure: Due to myocardial hypoxia, edema, and oliguria, patients are very sensitive to digitalis preparations. Even with small amounts, it is easy to produce poisoning, so it should be used with caution. The main treatment should focus on diuresis, salt restriction, water restriction, and vasodilation. In case of pulmonary edema, in addition to diuresis and vasodilation, oxygen should be administered under pressure, and morphine 0.1-0.2mg/kg can be injected subcutaneously. Bloodletting or tourniquet should be applied to the limbs, and dialysis may be necessary if required.

　　Hypocalcemia: Intravenous administration of 10% calcium gluconate 10ml, 1-2 times a day, and appropriate sedatives such as Valium can be added.

　　(2) Treatment during polyuria period:

　　A. Correction of hypokalemia: Increased urine output can easily lead to hypokalemia due to potassium excretion in the urine. Oral administration of 2-3mmol/(kg·d) can be given, and if hypokalemia is marked, intravenous supplementation can be used, with a concentration generally not exceeding 0.3%. Add 3ml of 10% KCl to 100ml of liquid, and always monitor blood potassium concentration or ECG changes to prevent hyperkalemia.

　　B. Water and sodium supplementation: Due to the large loss of diuretic water, attention should be paid to supplementation, but if there is excessive urine output, the intake of water should be appropriately restricted, preferably 1/2-2/3 of the urine output, as excessive fluid administration will prolong the polyuria period.

　　C. Control of infection: About 1/3 of patients die from infection, so it should be actively controlled. Sensitive antibiotics can be chosen, but attention should be paid to protect renal function.

　　D. Dialysis treatment: Early dialysis can reduce mortality. According to the specific situation, hemodialysis or peritoneal dialysis can be selected. Indications for dialysis:

　　a. Blood biochemical indicators: BUN>28.56mmol/L (80mg/dl); Cr>530.4?mol/L; blood potassium>6.5mmol/L or ECG shows hyperkalemia; CO2CP

　　b. Clinical symptoms of uremia are obvious, oliguria for 2-3 days, frequent vomiting, with peripheral neuropathy or psychiatric symptoms.

　　c. Marked water and sodium retention.

　　d. Poisoning by chemical substances or drugs.

　　2. Severe circulatory congestion: mainly diuretics, and if there is significant hypertension, vasodilators such as sodium nitroprusside 1-2?g/(kg·min) can also be tried. Digitalis is generally not used. When heart failure is marked, low-dose application of digitoxin (cedilanide) 0.01mg/(kg·time) can be used, usually 1-2 times, without the need for maintenance medication. If the above treatment is ineffective, hemofiltration, hemodialysis, or peritoneal dialysis can be used for treatment.

　　Severe circulatory congestion, heart failure: bed rest should be maintained, strict restriction of water and sodium intake, and prompt diuresis and antihypertensive treatment should be carried out.

　　Strong diuretics: furosemide (Lasix) 2mg/kg intravenous injection, repeatable after 4-6 hours. If there is still no urine, the dose can be increased to 3-4mg/kg. Most patients start diuresis on the 7th to 10th day of the disease course. However, if there is still no urine, if BUN increases by 7.2-18mmol/L (20-50mg/dl) or Cr increases by 176.8-265.2?mol/L (2-3mg/dl) within 24 hours, or if there is excessive cardiac load or hyperkalemia, acidosis that cannot be corrected, dialysis therapy should be adopted.

　　Patients with obvious pulmonary edema can be treated with vasodilator drugs such as sodium nitroprusside (administered in the same way as for hypertensive encephalopathy) or phentolamine 0.1-0.2mg/kg added to 10%-20ml of 5%-10% glucose solution for intravenous slow injection to reduce the cardiac load. For restlessness and anxiety, sedatives such as pethidine (diphenhydramine) (1mg/kg) or morphine (0.1-0.2mg/kg) can be administered subcutaneously. After observation, the cardiac output of such patients is not low, the difference in arterial-venous oxygen saturation is reduced, and the ejection fraction is not low, so it is generally not recommended to use digitalis preparations. Circulatory congestion that is still difficult to control after the above treatment can be treated with peritoneal dialysis or hemofiltration.

　　3. Hypertensive Encephalopathy: Sodium nitroprusside (sodium nitroprusside) intravenous infusion is the first choice, with a dose of 1 to 5?g/(kg·min). It should not be used after 4 hours, and the infusion should be protected from light. The main adverse reactions include nausea, vomiting, headache, muscle spasms, and hypotension. Diazoxide (3 to 5 mg/(kg·time)) or nicardipine (perindopril) (0.5 to 6g/(kg·min)) can also be used for intravenous injection. For convulsions, diazepam (diazepam; valium) 0.3mg/(kg·time) intravenous injection or phenobarbital (phenobarbital) 5 to 8mg/(kg·time) intramuscular injection can be used for treatment.

　　Fifth, Adrenal Cortical Hormone Treatment

　　Adrenal cortical hormones should be avoided in general patients to prevent exacerbation of water and sodium retention and hypertension. For children with persistent large amounts of proteinuria or clinical and pathological trends towards chronicity, oral prednisone (prednisone) treatment can be considered, with a dose of 1 to 2 mg/(kg·d) and a gradual reduction in dosage. The course of treatment is usually 1 to 2 months. For patients with a large number of crescents in renal biopsy, initial methylprednisolone (methylprednisolone) pulse therapy at 20 to 30 mg/(kg·time) can be administered, followed by oral prednisone treatment.

　　Sixth, Treatment during the Recovery Period After the disappearance of gross hematuria, edema, and hypertension, traditional Chinese medicine such as Liuwei Dihuang Wan (6g per time, 3 times a day) or Bai Mao Gen (20g per time, decocted for administration) can be used for treatment until microscopic hematuria disappears.

　　Prognosis

　　The prognosis of acute glomerulonephritis in children is good, most of whom can recover completely. The main cause of death during the acute stage is severe complications. The vast majority of children will have gross hematuria disappear within 2 to 4 weeks, with an increase in urine output, the subsidence of edema, and a gradual recovery of blood pressure. The residual proteinuria and microscopic hematuria will disappear more than 6 months later. A few severe patients may last for 1 to 3 years, even developing into chronic nephritis or chronic renal insufficiency.