What Is Post-streptococcal Glomerulonephritis?

Glomerulonephritis after acute streptococcal infection

Glomerulonephritis after acute streptococcal infection

Glomerulonephritis after acute streptococcal infection is often referred to as acute nephritis. In a broad sense, it refers to a group of etiologies and pathogenesis of different types, but clinical manifestations of acute onset, glomerular disease characterized by hematuria, proteinuria, edema, hypertension and decreased glomerular filtration rate, so also Often called glomerulonephritis after acute streptococcal infection. This disease is the most common kidney disease in childhood. It is more common in the age of 3 to 8 years, and rare under 2 years. The male to female ratio is approximately 2: 1.

Name of glomerulonephritis after acute streptococcal infection

Glomerulonephritis after acute streptococcal infection

Classification of glomerulonephritis after acute streptococcal infection

Nephrology

Diagnosis of glomerulonephritis after acute streptococcal infection

Should be noted with hemolytic uremic syndrome, aggressive glomerulonephritis, nephrotic nephrotic syndrome, benign recurrent hematuria, hereditary familial nephritis, allergic purpuric nephritis, lupus erythematosus nephritis, urinary system infection, or viral Nephritis identification.

Clinical manifestations of glomerulonephritis after acute streptococcal infection

The clinical manifestations of this disease vary from mild to subclinical, with clinical symptoms not obvious, and severe renal failure with severe severity. Most patients have a history of precursor infection. The incubation period for streptococcus infection in the upper respiratory tract is 1-2 weeks, and the incubation period for streptococcal skin infection is 3-4 weeks. Mild patients have no significant history of infection, only the anti-streptolysin "O" titer increases, and the degree of nephritis does not depend on the severity of the precursor infection. The typical symptoms are acute onset after asymptomatic incubation period of 1-3 weeks after prodromal infection, manifested as acute nephritis syndrome, mainly including hematuria, proteinuria, edema, oliguria, hypertension and renal failure.

1. Hematuria is usually the first symptom of onset. Almost all patients have hematuria, 40% of which is gross hematuria. The urine color is uniform brown, turbid, or meat-washing water-like, but no blood clots, acidic urine can be a soy-like tan, lasting 1-2 weeks, and hematuria under the microscope can last for 1-6 months. It lasted for six months or more, but the majority recovered.

2. Almost all patients with proteinuria have varying degrees of proteinuria, but most of them are less than 3.0g / d, a few more than 3.5g / d, often non-selective proteinuria. Urine protein has been transferred to a small amount at the time of consultation.

3. Edema is often the early symptoms of onset, the milder is eyelid edema in the morning, showing the so-called "nephritis face". In severe cases, it can extend to the whole body, with a slight concavity, and a few may have nephrotic syndrome. If the edema continues to develop, it often indicates a poor prognosis.

4. Hypertension occurs in 70% to 80% of patients, most of which are mild and moderate blood pressure increase, and occasionally severe hypertension. Generally, the recovery is rapid, and the degree of hypertension and edema are often parallel, and it returns to normal with diuretic swelling. If the blood pressure continues to rise for more than 2 weeks and there is no downward trend, it indicates that the renal disease is more serious.

5. Most patients with oliguria have decreased urine output (<500ml / d) at the onset of the disease and are accompanied by transient azotemia. After 2 weeks, urine output gradually increases and renal function recovers.

6. Rarely, renal dysfunction develops from oliguria to anuria, and urea nitrogen and blood creatinine slightly increase. If urea nitrogen 21.4mmol / L (60mg / L), creatinine 352mol / L (4.0mg / L) Should be alert to the occurrence of acute renal failure.

7. Patients with systemic manifestations often have fatigue, anorexia, nausea, vomiting, dizziness, headache, and occasionally coexist with rheumatic fever. The lightest subclinical patients only had microscopic hematuria, and even urine tests were normal. Only blood C3 changed regularly, and the acute phase decreased significantly, recovering in 6-8 weeks. Renal biopsy has typical pathological changes. disease

Glomerulus

Etiology Acute glomerulonephritis often develops after infection. The most common pathogenic bacteria is -hemolytic streptococcus, which is occasionally found in staphylococci, pneumococcus, typhoid, diphtheria, and protozoa such as malaria parasites, schistosomiasis, and viruses.

Clinical study of glomerulonephritis after acute streptococcal infection

Glomerulonephritis is most common clinically after acute streptococcal infection. AGN is common in pharyngeal or skin group A beta-hemolytic streptococcal infections, and it is rarely secondary to other infections (such as staphylococci, pneumococcus, group C streptococci, viruses, or parasites). The exact pathogenesis of pathophysiological AGN is unknown, and it is known to be an immune complex disease in the acute phase. It is marked by the formation of antibodies against streptococcal antigens and the covering of the kidney with complement immune complexes. AGN only occurs after -hemolytic streptococcal infection in group A. The latter is called a nephritogenic strain, and the typical antibody to the nephritogenic strain is directed against its cell wall antigen M type 1, 2, 4, 12, 18, 25, 49, 55, 57, 60. AGN is considered to be immune-mediated immune complex disease. There are three evidences: the incubation period after streptococcal infection is equivalent to the time when the body produces immunity after the first infection; the circulating immune complex is positive in the early stage of the disease, and serum complement is decreased; Immunofluorescent IgG and C3 were granular in the glomerular mesangial area and capillary loops. But how to cause progressive renal damage and eventually glomerulosclerosis is not clear.

Studies have shown that all types of proliferative glomerulonephritis have obvious glomerular and interstitial inflammatory cell infiltration, while non-proliferative glomerulonephritis has only a small amount of inflammatory cell aggregation. In proliferative glomerulonephritis, the infiltration of monocytes and T lymphocytes in the glomeruli is significantly increased, which is related to the severity of proteinuria. The glomerular immune deposits can activate the complement system, which is mediated by inflammatory cells and participates in the immune response that causes nephritis. Moreover, the pathogenic nature of the complement system clearly includes cell-independent mechanisms. For example, the production of C3a, C5a and allergic toxins results in the release of histamine, resulting in increased capillary permeability. The C5b-C9 complex (membrane attack complex), the terminal component of complement, has a direct effect on the basement membrane of glomerular capillaries. The non-dissolving effect of C3a-C5a components can stimulate platelets to secrete serotonin (5-hydroxytryptamine) and thromboxane B; stimulate macrophages to secrete phospholipids and arachidonic acid; stimulate mesangial cells to secrete prostaglandins, proteolytic enzymes, and phospholipases And oxygen free radicals and so on constitute inflammatory mediators. These inflammatory mediators can cause glomerular inflammatory lesions.

Evidence supports the idea that one or more streptococcal antigens that have affinity for the glomerular structure are implanted into the glomerulus at the early stage of streptococcal infection, and then antibodies produced by the host immune response bind to the antigen 10 to 14 days later , Leading to the occurrence of disease. The most likely candidate antigens include: Streptococcus nephropathy strain-associated proteins (which inhibit streptokinase activity) and nephritis binding proteins (precursors of pyrogenic exotoxin B). Although the concentration of circulating immune complexes is not related to the severity of the disease, it may be in the initial formation of in situ immune complexes, the occurrence of a large number of glomerular immune deposits, and changes in the glomerular basement membrane permeability. kick in.

Complications of glomerulonephritis after acute streptococcal infection

1. Severe circulatory congestion and heart failure due to water and sodium retention, clinical signs of water overload may appear, such as

Proteinuria

Severe edema, circulatory congestion, heart failure, and pulmonary edema. The main manifestations are shortness of breath, inability to lie flat, chest tightness and cough, wet snoring at the base of the lungs, enlarged heart, enlarged liver, accelerated heart rate, galloping rhythm, etc. Early signs of circulatory congestion usually relieve with diuretic effects within 1-2 weeks.

2. The domestic reported incidence of hypertension encephalopathy is 5% to 10%, and the general blood pressure exceeds 18.7 / 12kPa. At the same time, it can be diagnosed if it is accompanied by one of the three symptoms of visual impairment, convulsions, and coma. Often manifested as severe dizziness, vomiting, lethargy, unconsciousness, darkness, and severe cases with paroxysmal convulsions and coma. Fundus examination is common for retinal arteriolar spasm, bleeding, exudation, and disc edema.

3. The incidence of acute renal failure is 1% to 2%, which is characterized by oliguria or anuria, increased blood urea nitrogen, varying degrees of hyperkalemia and metabolic acidosis and other changes in uremia.

Scientific diagnosis of glomerulonephritis after acute streptococcal infection

Diagnosis: Acute nephritis with typical clinical symptoms is not difficult to diagnose. The main diagnostic basis is:

1. A history of significant streptococcal infection before the disease. Typical hematuria, proteinuria, oliguria, and edema appear clinically.

Chest radiograph

, Hypertension and other acute nephritis syndrome.

2. Streptococcus culture and serological examination The culture of pharynx or skin pus secretions showed positive A group hemolytic streptococcus, serum complement decreased, and serum ASO increased to confirm the diagnosis. Patients with atypical clinical manifestations need to make a diagnosis based on urine tests and changes in serum complement dynamics. Because 90% of glomerulonephritis patients with acute streptococcal infection have hypocomplementemia, serum complement determination can be used as a first-line test to evaluate acute nephritis.

Test method for glomerulonephritis after acute streptococcal infection

Laboratory examination of glomerulonephritis after acute streptococcal infection

1. Urine routine examination and microscopy showed a significant increase in red blood cells, and urine sediment examinations showed 10 red blood cells at full field / high power. Granular casts, erythrocyte casts, renal tubular epithelial cells, and white blood cells; urinary proteins (+) to (+++) can also be seen. Such changes in urine routine often last for months. Fibrin degradation products (FDP) can also appear in the urine.

2. Blood tests commonly include orthochromic and orthocytic anemia. Hemoglobin is generally between 100 and 120 g / L, which is mainly related to water and sodium retention, blood dilution, and is equal to the degree of uremia. The white blood cell count is normal or increased, and the erythrocyte sedimentation rate usually increases rapidly. Renal function tests show a decrease in glomerular filtration rate (GFR) in the acute phase. Some patients may have significant azotemia, BUN and Scr in blood may increase, hyperkalemia, dilute hyponatremia, high Chloric acidemia, decreased plasma protein. In severe cases, if there is oliguria, anuria or acute renal insufficiency, significant azotemia can be seen, with metabolic acidosis and electrolyte disturbances; but the renal tubular function changes slightly.

3. Bacteriological and serological examinations In patients not treated with antibiotics, about half of the pharynx or skin pus secretions were cultured to be positive for group A hemolytic streptococcus. In approximately 70% of patients, the titer of serum anti-streptolysin "O" (ASO) is> 400U. After the in vitro antigen component of Streptococcus enters the human body, it can stimulate the body to produce corresponding antibodies. This antibody can be used as evidence of recent streptococcal infections. Commonly used are anti-streptolysin "O" and "S" (ASO, ASS), anti-streptococcal kinase, hyaluronidase, and anti-DNAM enzyme B. Among them, ASO is widely used in clinical. After 3 weeks of streptococcal infection, the titer increased (> 1: 200), reached a peak in 3 to 5 weeks, and then gradually decreased, and about half returned to normal within 6 months. Serum ASO and anti-DPNase titers are low after pyoderma, and the positive rates of antihyaluronidase (ASH) and anti-DNase are higher.

Complement level measurement showed that complement C3 and CH50 properdin in most patients decreased, C3 <0.8mg / ml, and returned to normal more than 6-8 weeks after illness. If the complement continues to decline without returning to normal, it should be suspected of mesangial capillary nephritis or other systemic diseases (SLE, etc.). In some cases, the circulating immune complex (CIC) test was positive and cryoglobulinemia. Increased fibrinogen, factor VII, and cytosin activity in blood.

4. Blood biochemical examination For patients with severe edema and large amounts of proteinuria, the total plasma protein, albumin / globulin ratio, blood cholesterol, triacylglycerol, and lipoprotein should be determined to determine whether there is hypoproteinemia and Hyperlipidemia.

5. Detect antinuclear antibodies, anti-double-stranded DNA antibodies, anti-Sm antibodies, anti-RNP antibodies, and anti-histone antibodies to exclude systemic lupus erythematosus.

6. Examination of liver function and hepatitis B virus infection markers exclude hepatitis B nephritis.

Other auxiliary examinations of glomerulonephritis after acute streptococcal infection

1. The plain X-ray of the abdomen shows that the renal shadow is normal or enlarged.

2. Chest X-ray photo The heart may be normal or slightly enlarged, often accompanied by pulmonary congestion.

3. Kidney biopsy

(1) Under the light microscope, the glomeruli are enlarged, the cellular components are increased, the vascular loops are enlarged, the endothelial cells are swollen, the mesangial cells and mesangial matrix are proliferated, and the capillaries are blocked to varying degrees. In addition, it is often accompanied by exudative inflammation.

B-ultrasound

Run. Due to the different degrees of proliferation and exudation, only a part of the mesangial cells proliferate in the light; the endothelial cells also proliferate in the severe, and can partially or completely block the capillaries; more severe ones form a crescent. Extensive crescent formation was observed in patients with clinical manifestations of rapid progress.

(2) Electron microscopy: typical hump changes of the disease can be seen under the epithelium (that is, fine particles of electron dense deposits under the epithelium). Humps usually disappear 6 to 8 weeks after the illness.

(3) Immunofluorescence examination: Diffuse granular IgG, C3, properdin, and fibrin-associated antigen deposits were seen along the capillary loops and mesangial regions. Occasionally, IgM, IgA, C1q, and C4 were deposited. The indications for renal biopsy of this disease are: oliguria for more than 1 week or progressive decrease in urine output with worsening renal function and the possibility of progressive nephritis; the condition does not improve within 2 to 3 months after the onset, and is still high Blood pressure and persistent hypocomplementemia; Acute nephritis syndrome with nephrotic syndrome. Differential diagnosis 1. Systemic infectious fever disease When various infections cause fever, renal blood flow and glomerular permeability may increase, and transient proteinuria may also occur. This change occurs in the early stages of high fever and infection, and regression Urine returned to normal after the fever, without other symptoms of acute nephritis syndrome.

B-ultrasound

2. Multiple primary glomerular diseases manifested by acute nephritis syndrome

(1) Mesangial capillary nephritis: The onset process is similar to this disease, but hypocomplementemia lasts longer, and the disease has no tendency to heal. A large amount of proteinuria and persistent hypocomplementemia are characteristics of this disease. Renal biopsy can clearly identify the differential diagnosis.

(2) Acute nephritis: The onset is similar to acute nephritis, but the symptoms are more severe, mostly progressive oliguria, anuria, and the condition develops rapidly. Renal failure soon appears. Renal biopsy can be diagnosed in time and related to the disease. Identification.

(3) IgA nephropathy: more than 1 to 3 days after acute upper respiratory tract infection, hematuria, or proteinuria, serum complement is normal, blood IgA levels can increase, and the disease is easy to relapse.

3. Acute episodes of chronic glomerulonephritis. These patients often have a history of kidney disease and similar episodes. They quickly develop infection after infection, have no incubation period, and are often accompanied by anemia, persistent hypertension, and renal insufficiency. B-ultrasound showed shrinkage of both kidneys.

4. Systemic systemic diseases Systemic lupus erythematosus nephritis, allergic purpura nephritis can appear acute nephritis syndrome, these two diseases have obvious skin lesions and arthritis symptoms such as joint pain, the former lupus cells in blood and anti-DNA Antibodies were positive and the latter were positive for the beam arm test. Just ask the medical history in detail and make the relevant examination to make the correct diagnosis.

Treatment of glomerulonephritis after acute streptococcal infection

Glomerulonephritis clears infected foci after acute streptococcal infection

About 10 days of penicillin, those who are allergic to penicillin can use erythromycin or cephalosporins. Patients with local abscesses should undergo surgical drainage immediately.

Limiting water intake in the acute phase of glomerulonephritis after acute streptococcal infection

Calculated by intangible dehydration [350ml / (m2.d)] plus daily urine output and daily abnormal loss (vomiting, diarrhea, etc.). Encourage eating, low salt, low protein, carbohydrate-based.

Glomerulonephritis hypertension and hypertensive encephalopathy after acute streptococcal infection

Bed rest for mild hypertension, oral reserpine 0.02 0.03mg / kg each time, diuretic dihydrochlorothiazide 1 2mg / (kg.d), blood pressure measurement 1/4 6h, control blood pressure in a safe range [ Diastolic blood pressure <12kPa (90mmHg), systolic blood pressure <18.6kPa (140mmHg)]. For severe cases with diastolic blood pressure> 12kPa (90mmHg), reserpine 0.07mg / kg (not more than 2mg each time), orally or intravenously, intramuscularly for 1 / 8-12 hours. Hydrazine should be used at the same time 0.1mg / kg, intramuscularly or slowly intravenously, or 0.5mg / kg orally. If the blood pressure is effective within 2 to 3 hours, it can be repeated as appropriate, but reserpine should not be used more than 3 times. If convulsions occur in hypertension, a rapid intravenous injection of diazoxide 5-10 mg / kg, or an intravenous injection of methyldopa 10-20 mg / (kg.d), or an oral injection of methyldopa 20-40 mg / (kg. d), orally divided into 4 times; or combined with dihydrochlorothiazide 2.5mg / (kg.d) and hydrazine phthalazine 2 ~ 4mg / kg, taken 3 times, instead of injection, to reduce blood pressure to a safe range; Available sodium nitroprusside 1 2g / (kg.min), such as adding 5 20mg sodium nitroprusside to 100ml of 10% glucose solution for intravenous drip, about 10 drops / min for children, adjust the speed according to the antihypertensive effect. Blood pressure is often observed during the infusion. If the blood pressure drops to normal, the drug should be discontinued.

Acute glomerulonephritis after acute streptococcal infection

In patients with sudden left heart failure and pulmonary edema, the amount of fluid and sodium is mainly limited. Controls hypertension, diuresis, and lowers blood volume. After inhaling oxygen through 50% to 75% ethanol, morphine is sedated (but disabled in respiratory failure, coma, and shock); vasodilators such as phentolamine + alamin are used. Phentolamine 0.5 1mg / kg, alamin is half the amount of phentolamine, intramuscularly or intravenously in 10ml glucose 10ml. Intravenous sodium nitroprusside can also be used. Cardiotonic drugs can be selected from fast-acting cardiotonic poisonous trichoside K or trichoside C. Diuretics can be sodium diurea 0.5mg / kg, 1 2 / d, or furosemide (fast urine), 1mg / kg, intravenous or intramuscular injection, 1 2 / d.

Acute glomerulonephritis after acute streptococcal infection

Diuretic mixture (caffeine 250mg, vitamin C3000 4000mg, aminophylline 125mg, procaine 300mg, 10% -25% glucose solution 500ml) can be used in children without obvious edema, hypertension or heart failure at the beginning stage. 10ml / kg each time, finished within 2h; or 0.5g / kg mannitol each time, intravenous injection. Those with obvious edema or high blood pressure and heart failure should use furosemide 1 2mg / kg each time. If the effect is not obvious, repeat it 2 3 times as appropriate. In addition to strictly controlling the fluid intake and maintaining a weight loss of 100-200g / d, the following measures are taken in each case:

(1) Management of hyperkalemia: potassium-containing foods, drugs and stock blood are prohibited. Regular insulin is 0.15U / kg, glucose is 0.5g / kg, and the mixed solution is dripped intravenously within 2h. 10% calcium gluconate 0.5 1ml / kg, intravenously infused within 10 15min after 1 time dilution. 5% sodium bicarbonate 3 ~ 5ml / kg, intravenous drip. Peritoneal dialysis or hemodialysis should be considered for serum potassium above 7mmol / L.

(2) Control of azotemia and correction of acidosis: Supply sufficient heat energy, reduce tissue catabolism, and prohibit hydrolyzed proteins. Anabolic hormones such as Nandrolone Phenylpropionate 12.5-25mg, intramuscular injection, every 2 days once. When the blood pH is less than 7.2 and the symptoms of acidosis, 5% sodium bicarbonate 5ml / kg can be used with caution to relieve symptoms; if the blood pH 7.2 has no clinical manifestations, it is not necessary to treat with sodium bicarbonate. Blood urea nitrogen 5.6mmol / L, endogenous creatinine clearance is reduced, creatinine and creatine are increased, blood potassium is too high, blood phosphorus is as high as 3.55mmol / L, or dialysis or hemodialysis should be performed when the water load is too heavy .

Glomerulonephritis after acute streptococcal infection

In western developed countries, the incidence of acute glomerulonephritis accounts for 10% to 15% of all glomerular diseases, and it is gradually decreasing. However, in Africa and some Asian countries with poor health conditions, the disease is a more common histological type of primary kidney disease. More than 70% of patients in northern China occur after streptococcal infection of the respiratory tract, which is more common in spring and winter; more often in the south than in summer after pustular disease. Age: It can occur at any age, and it is most common in children 2 to 12 years old. Patients younger than 2 years are rare (<5%), and fewer than 40 years old, 5% to 10%. Gender: The ratio of male incidence to female is 2: 1. Genetic: The connection between human leukocyte antigen (HLA) and glomerulonephritis after acute streptococcal infection is still inconclusive. Studies have shown that only DR4 is common in some unrelated patients. DR1 has been reported to be associated with the disease, while people with Bw48 and DRw8 are relatively less susceptible to the disease.

Prevention of glomerulonephritis after acute streptococcal infection

This disease is a self-limiting disease and lacks specific therapies. Although the prognosis is poor, it is not incurable. There are many drugs available for the treatment of this disease, but the efficacy is still controversial. Rest and symptomatic treatment are essential for clinical recovery. The acute phase is mainly to prevent and treat water and sodium retention, control circulating blood volume, maintain water and electrolyte balance to reduce symptoms, prevent the occurrence of serious complications (heart failure, acute renal failure, hypertensive encephalopathy), and remove the aggravating renal disease. Factors that promote the repair of kidney function.

1. In the acute period of rest, you must rest in bed, wait for gross hematuria to disappear, edema subsides, and return to normal blood pressure before you can gradually increase your activity. It is advisable to avoid heavy physical activity within 3 months.

2. Diet provides a low-salt diet rich in vitamins to ensure sufficient calories. Appropriate supplement

hematuria

For high-quality protein (proteins containing essential amino acids, such as milk and eggs), the amount of protein should be kept at 1g / (kg? D). For those with azotemia, the amount of protein should be limited to about 0.6g / kg per day. Such patients should limit potassium-containing foods. Patients with edema and hypertension should have a diet without salt or low salt until diuresis begins, and those with severe edema with little urine should limit the amount of water.

3. Treatment of infections In the treatment of acute nephritis, antibiotics for streptococci such as penicillin or macrolides are generally recommended. Especially when the bacterial culture is positive, antibiotics should be actively applied to prevent the spread of the bacteria. Most scholars still advocate the use of drugs such as penicillin and roxithromycin, even if the culture result is negative, and generally use it for 2 weeks or until cured. Some people still suggest that anti-infective treatment should be continued through the winter after the cure. On the one hand, it can control hidden lesions, and on the other hand, it can prevent other bacteria or streptococcus non-nephritis beads from causing new infections and avoid nephritis worsening and affecting renal function. For those who have a disease that lasts for more than 2 to 6 months, the condition does not heal repeatedly, and the tonsil lesions are obvious, a tonsillectomy can be considered.

4. Symptomatic treatment

(1) Diuretic and swelling: The main pathophysiological change of acute nephritis is the retention of water and sodium, and the increase in extracellular fluid volume, leading to clinical complications such as edema, hypertension, circulatory overload, and heart and renal insufficiency. Application of diuretics Not only to achieve swelling and diuretic effect, but also to help prevent complications.

Mild edema: no obvious renal damage, no serous fluid (pleural effusion, ascites). Commonly used thiazide diuretics, such as hydrochlorothiazide 25-50mg, 1 or 2 times / d. Such diuretics act on the distal tubules, but when the GFR is 25ml / min, they often cannot produce a diuretic effect. At this time, diuretics can be used.

Moderate edema: with renal function damage and a small amount of serous cavity effusion, first use thiazide diuretics, such as hydrochlorothiazide 25-50mg, 1 or 2 times / d. But when the GFR is 25ml / min, you can add diuretics, such as furosemide (fast urine) and etaneric acid (diuretic acid), furosemide (fast urine) 20-40mg / time, 1-3 Times / day, if the oral effect is poor, it can be administered intramuscularly or intravenously. It takes effect within 30 minutes, but the effect is short and can be used repeatedly. These two drugs still have a diuretic effect when the glomerular filtration function is severely impaired and the creatinine clearance is 5-10 ml / min. It should be noted that large doses can cause serious damage to hearing and kidneys.

Severe edema: When the daily urine volume is less than 400ml, there is a large amount of pleural effusion, ascites with renal impairment, (even acute renal failure) and complications such as hypertension and heart failure, immediately apply high-dose strong diuretics, such as furfur Semimi (fast urine) 60-120mg slow intravenous bolus, but the dose cannot be more than 400-1000mg / d, because the drug is too large, it can not increase the diuretic effect, but it will significantly increase adverse reactions, leading to irreversible deafness. If the diuretic effect is still unsatisfactory, blood purification therapies, such as hemodialysis or peritoneal dialysis, should be considered instead of risky overdose of diuretics.

Other diuretic and dehydrating drugs: Mercury diuretics may have renal parenchymal damage, osmotic diuretics such as mannitol can increase blood volume, aggravate cardiovascular and cerebrovascular accidents, and have the potential to induce acute renal failure; potassium-sparing diuretics Causes elevated blood potassium and should not be used when urine is low. For those with hyperuricemia, diuretics should be used with caution. In addition, vascular antispasmodics, such as dopamine, can be used for diuretic purposes.

5. Application of antihypertensive drugs Blood pressure does not exceed 18.7 / 12kPa (140 / 90mmHg) can be temporarily observed. If the blood pressure is still high after rest, water restriction, diuresis, antihypertensive drugs should be given. Antihypertensive drugs can be selected according to the degree of hypertension and the onset of emergency:

(1) Hydrazine (Hydrazine): This medicine can expand resistance blood vessels and reduce the heart's afterload. The oral dose is 25mg, 2 times / d, intramuscular injection of 0.15mg / kg every 12 to 24 hours; intravenous injection of 0.15mg / kg, repeated every 30 to 90 minutes, the maximum dose is 1.7 per day 3.6mg / kg, changed to oral after improvement. Intravenous injection can take effect immediately, reach the highest peak in 20 40min, and maintain hypotensive effect for 4 12h. Its main side effects are headache, increased heart rate, and gastrointestinal irritation.

(2) Calcium channel blockers: such as nifedipine (nifedipine), by blocking the entry of calcium ions into the cell, it interferes with the excitation-contraction coupling of vascular smooth muscle, reduces peripheral vascular resistance and reduces blood pressure, and can Better maintain heart, brain, and kidney blood flow. Oral or sublingual absorption and absorption is good, 10mg each time, blood pressure drops for 20min, the effect reaches a peak in 1 ~ 2h, lasts for 4 ~ 6h, combined with -blockers can improve the efficacy and reduce the heart rate caused by it . This medicine has a short half-life and requires multiple doses. A variety of long-acting preparations such as amlodipine and felodipine (bovidin), which are widely used in clinical applications and have good effects, can be selected as appropriate.

(3) Angiotensin-converting enzyme inhibitors: By inhibiting the activity of angiotensin-converting enzyme I, and inhibiting angiotensin dilation of small arteries, it is suitable for renin-angiotensin-aldosterone system-mediated hypertension. It is also available In patients with heart failure, the commonly used drug is captopril (mercaptoproline), which is administered orally at 25 mg and has an effect in 15 minutes. It has a better effect on renin-dependent hypertension.

(4) 1-receptor blockers: prazosin has vasodilator effect, which can reduce the load before and after the heart. It should be started from a small dose and gradually increased. Side effects include orthostatic hypotension, dry mouth, dizziness and fatigue. Wait.

(5) Diazoxide (low pressure azole, chlorobenzthiadiazine): a non-diuretic thiazine derivative, which can quickly lower blood pressure in patients with severe hypertension or hypertensive encephalopathy, and maintain it for a long time, No continuous drip is needed, and it is more convenient to apply. Adult 50 100mg, rapid intravenous injection (10 ~ 15min injection completed), 1 2min effect, 2 5min effect is strongest, lasting 4-12h, in order to prevent water and sodium retention, 30 60min before each injection Furosemide 0.5 1mg / kg (orthostatic hypotension may occur due to combined use with furosemide, which is contraindicated in patients with angina pectoris and heart failure). Can be repeated after 30 minutes. The antihypertensive effect is related to the dose and injection speed. A rapid intravenous injection of a sufficient amount of medicine can obtain a sufficient antihypertensive effect. Side effects are water and sodium retention and elevated blood sugar.

(6) Sodium nitroprusside: used in patients with severe hypertension. Dosage was continued intravenously at a rate of 1 g / (kg? Min). Works within seconds. Usually 5 to 20mg is dissolved in 100ml glucose solution for intravenous drip, starting with a small dose, and adjusting the drip rate according to blood pressure. This medicine has the advantages of fast action, high efficacy and low toxicity. It acts on both the arterial resistance vessels and the venous volume vessels. It can reduce peripheral resistance without increasing venous return, so it is especially suitable for patients with heart failure. . Medicines should be prepared fresh, and the infusion bottles should be wrapped in black paper to protect from light.

6. Treatment of serious complications

(1) Treatment of acute circulating congestive state and acute congestive heart failure: strictly stay in bed, limit the amount of sodium and water. Diuretics are used. When heart failure occurs, digoxigenin or strophanthin K can be used. In critically ill patients, the upper and lower extremities or venous blood can be restrained by rotation (150 to 300 ml each time) to reduce venous blood return and reduce the burden on the heart. Pulmonary congestion. Phenyltolamine (rigitin) or sodium nitroprusside can reduce the load before and after the heart. When conservative treatment is not effective, peritoneal dialysis or hemofiltration dehydration can be used.

(2) Treatment of hypertensive encephalopathy: The above drugs are used for active antihypertensive treatment. The preferred dose of sodium nitroprusside is 5 mg and 10% glucose solution in 100 ml intravenous drip. Starting at 4 drops / min, blood pressure should be monitored during medication, blood pressure should be measured every 5 to 10 minutes, and the dose should be adjusted according to blood pressure changes. The maximum is 15 drops / min, which is 1 to 2 / (kg? Min), the total daily dose < 100g / kg, the drug should be protected from light, intravenous drip within 4h should be completed, if the pharmaceutical solution> 4h, it should be reconstituted. After treatment, if the patient's hypertensive encephalopathy is relieved, his mind is improved, and his convulsions are stopped, other antihypertensive drugs should be used to maintain normal blood pressure. Because hypertensive encephalopathy can be life-threatening, you should quickly lower your blood pressure and race against time. Sodium nitroprusside has fast onset and short half-life. It can be effective in 1 to 2 minutes, and the effect disappears after 1 to 10 minutes of withdrawal without drug dependence. However, it should be noted that sodium nitroprusside can produce thiocyanate metabolites, so intravenous drug concentration should be low, drip rate should be slow, application time should be short (<48h), and blood pressure should be closely monitored. The effective circulating blood volume is too low, which results in a decrease in renal blood flow and damage to renal function. Rescue acute nephritis complicated by hypertension crisis, sodium nitroprusside is reliable, safe, and has few side effects. With cerebral edema, strong diuretics and dehydrating agents should be used. The treatment of reducing intracranial pressure and dehydration should be 20% mannitol, 5ml / kg each time, intravenous injection or intravenous drip; dexamethasone 0.3 ~ 0.5mg / kg (or 5 ~ 10g / time), every 6 ~ Intravenous infusion at 8 hours; Furosemide 1 mg / kg intravenous infusion, dehydration and diuresis every 6-7 hours; If convulsions, pay attention to symptomatic and stop spasm, and those who continue to twitch, can use sedative drugs such as diazepam (Diazepam) 0.3mg / kg each time, the total amount does not exceed 10 ~ 15mg intravenously; or chloral hydrate retention enemas or phenobarbital intramuscular injection, and can be supplemented with oxygen.

7. Dialysis treatment This disease can be used in the following two cases: acute urinary failure with oliguria, especially when hyperkalemia; severe water and sodium retention, causing acute left heart failure, dialysis ultrafiltration dehydration For effective measures, the condition can be alleviated. It is worth noting that this disease should not be treated with glucocorticoids, non-steroidal anti-inflammatory drugs (such as indomethacin), and anisodamine drugs.

Traditional Chinese medicine treatment of glomerulonephritis after acute streptococcal infection

Traditional Chinese medicine theory of traditional Chinese medicine believes that in the acute phase of the disease, there are wind-cold syndrome, wind-heat syndrome, damp-heat syndrome, and cold-dampness syndrome; in the recovery period, there are yin deficiency and qi deficiency. According to medical history, edema and systemic symptoms, it can be treated according to syndrome differentiation. The principle of treatment in the acute phase is to eliminate evil. It is advisable to declare lungs and water, clear heat and cool blood, and detoxify and dampen dampness. In the recovery period, it is mainly to correct and eliminate evil. The evidence is divided as follows:

Acute glomerulonephritis after acute streptococcal infection

Wind-cold syndrome: manifestation of edema that spreads quickly from the eyelids to the entire body, with head and face swelling, bright skin color, less urine, redness, slight cold or fever, joint pain, nasal congestion, cough, or shortness of breath, pale tongue Thin white with tight pulses. The ruler of the law dredged the wind and dispersed the cold, and passed through the Yangshui River. Prescription medicine commonly used drugs: ephedra, almond, windproof, cinnamon sticks, Poria, Poria, Poria, Alisma, Atractylodes, Psyllium, etc. Cough, shortness of breath, add gardenia, perilla, shoot dry, mulberry skin, etc .; external cold proves obvious, painful joints, pain, add live, thresh leaf; blood pressure rises significantly, remove ephedra, add vine, achyranthes, prunella ; Wind and cold combined with heat,

Wind-heat syndrome: sudden head and face eyelid edema, fever, sweating, dry or thirsty throat, sore throat, redness and redness, red tongue, thin yellow fur, slippery pulses or floating numbers. The main formula of the law is to relieve wind and heat, and relieve swelling. Prescription use: commonly used medicines: honeysuckle, forsythia, burdock, eustoma, white grass root, plantain, raw ephedra, raw plaster, diarrhea, licorice and so on. Pharyngeal pharyngeal pain is obvious, plus isatis root, mangosteen root, Scutellaria baicalensis; high fever thirst, reuse of plaster and reed root; headache plus crocus, chrysanthemum; upset plus gardenia; severe hematuria plus size thistle, madder, and crane grass with cooling blood Hemostasis.

heat toxicity syndrome: manifestation of systemic edema, oliguria, redness of skin, sore throat, swelling of the mouth, bitter thirst, upset, or fever, constipation, red tongue, yellow fur, slippery pulses or floating numbers. This certificate is usually caused by skin sores, bloated or swollen throats, rot, and purulence. It is characterized by swelling of the whole body, short urination, constipation, mouth pain, thirst, upset, and red tongue and yellow fur. The main method of treatment is to clear heat and detoxify, and to dampen swelling. Application of prescriptions: Commonly used medicines: honeysuckle, wild chrysanthemum, purple sage, dandelion, Hedyotis diffusa, Scutellaria baicalensis, Baibagen, corn whisker, Poria cocos, etc. Edema was obviously added with duckweed, polyporia, plantain to clear heat and dampness; those with heavy hematuria and Xiaojiyinzi to cool the blood to stop bleeding; sore erosion plus Sophora flavescens, Coptis chinensis, Atractylodes lancea; skin eczema plus Sophora flavescens, white moss skin, Ground skin; constipation plus rhubarb; upset mouth with gentian and gardenia; swollen throat with mountain bean root and horse bob.

Damp-heat syndrome: This syndrome is common in the middle and late stages of the disease. After the edema is reduced or subsided, it can also be seen in the continuous stage of edema. It is characterized by hematuria, heavy head and body, dullness, dullness, sticky mouth, unpleasant bowel movements, yellow tongue and greasy fur. The main prescription of the law is to clear heat and dampness, cool blood to stop bleeding. Prescription use: commonly used medicines: Scutellaria baicalensis, talc, pork columbine, Bai Kouren, small thistle, fried Puhuang, light bamboo leaves, angelica, gardenia. Peeing is astringent with white hydrangea, stone reed, and money grass; headache and dizziness are added to vines and chrysanthemums; skin sores are removed from white cocoons, dandelions and purple flowers are added;

Cold and dampness syndrome: showing edema of the whole body, with swelling of the limbs and below the waist, accompanied by heavy drowsiness, drowsiness and dullness, turbid shortness of urination, pale tongue, white greasy tongue, and slow pulse. This card is more common in those who are weak or who have lived in a wet and wet environment for a long time. It is characterized by symptoms of wet and spleen soil such as swelling below the waist and drowsiness and appetite. The main prescription of the law is Tongyang Lishui, dampness and swelling. Prescription use: commonly used medicines: Atractylodes macrocephala, Guizhi, Poria cocos, Poria cocos, Laxative, Mulberry skin, Potbelly skin, Chenpi, Ginger skin, etc. The upper body is swollen or even coughing, plus ephedra, almonds, and Su Zi Xuanfei asthma; suffocation, abdominal distension, mulberry peel, thicken Pu, Chuanjiao, and self-protection; cold body limbs, slow pulse, add aconite, ginger.

Recovery phase of glomerulonephritis after acute streptococcal infection

(Symptoms disappear, only abnormal urine test) This period is gradually weakening of righteousness, and the stage of nostalgia, especially in the early stage of recovery. Most people advocate exorcism, and aromatization heat, clearing heat and diuresis are the main rules. Yin deficiency evil love, nourish yin and kidney, and clear away the heat.

Care of glomerulonephritis after acute streptococcal infection

1. According to pediatric general nursing routines and kidney disease nursing routines, those with heart failure will be administered according to heart disease nursing routines.

2. Rest in bed for at least 3 weeks. Patients with high blood pressure or heart failure should stay still until the edema completely disappears, and the heart, blood pressure and renal function completely return to normal.

3. Pay attention to urine output and color, pay attention to breathing, blood pressure, pulse, and inhale oxygen when breathing is difficult. If you have headaches, dazzling, vomiting, shortness of breath, pale face, irritability, oliguria, etc., you should report it to your doctor immediately.

4. According to the doctor's order, if there is obvious oliguria, edema or hypertension, the amount of sodium salt and protein should be limited.

5. Pay attention to oral hygiene and clean your mouth after every meal.

6. Accurately record the amount of entry and exit until the edema disappears and the urine output is normal.

Discharge criteria and follow-up:

Edema disappeared, blood pressure and erythrocyte sedimentation were normal, urine output and urine routine were normal or there was only a small amount of protein, occasionally red blood cells and stable for 2 weeks can be discharged. Regular outpatient review of general conditions, blood pressure, urine routine, and renal function review if necessary. Those requiring tonsil surgery can be performed in the third to fourth month of the recovery period.

Safety of glomerulonephritis after acute streptococcal infection

Avoid food: pickles, salted eggs, pickles, fermented bean curd, steamed buns (with soda or alkali), sea fish, rooster, pork head, goose, spinach, pepper, pepper, mustard, coffee.

Suitable foods: light, low protein, low salt, glucose, sucrose, broad beans

fresh vegetables

, Red bean, winter melon, watermelon, amaranth, malantou, chrysanthemum brain, turtle, cucumber, pig kidney, mung bean, garlic, carp, loofah, pumpkin, eggplant.

The intake of protein in the acute nephritis diet depends on the condition. At the beginning of the disease, the intake of protein should be limited. When the condition improves, the protein in the diet can gradually increase to the normal intake.

Add enough vitamins and eat more alkaline foods such as fresh vegetables and fruits to regulate the acid-base balance in the body and help the body recover. In the early stages of acute nephritis, when there is edema, oliguria, hypertension, or heart failure, the intake of salt and water is strictly restricted. After the edema is alleviated, urine volume and blood pressure return to normal, you can enter a low-salt diet; when the edema completely disappears, you can gradually transition to a normal diet.