Acute glomerulonephritis in children

Introduction to acute glomerulonephritis in children Acute glomerulonephritis (acuteglomerulonephritis) usually refers to glomerulonephritis (acutepoststreptococcal glomerulone phritis (APSGN) after acute streptococcal infection, which is caused by the deposition of immune complexes in the glomerulus caused by group A beta-hemolytic streptococcus. Diffuse glomerular capillary exudation, proliferative inflammatory lesions. The clinical manifestations vary in severity. Typical manifestations are edema, oliguria, hypertension, and a good prognosis. Most of them are fully recovered, and a few (1% to 2%) can be delayed and become chronic. basic knowledge The proportion of illness: 0.002% Susceptible people: children Mode of infection: non-infectious Complications: Hypertensive encephalopathy Acute renal failure Chronic nephritis

Causes of acute glomerulonephritis in children

Non-streptococcal infection (35%):

(including other Staphylococcus, Streptococcus, Gram-negative bacilli, etc.), viruses (influenza virus, Coxsackie virus B4, Epstein-Barr virus), Mycoplasma pneumoniae and protozoa, etc., in group A beta-hemolytic streptococcus, by the respiratory tract The strains of nephritis caused by infection are mainly type 12, a few are type 1,3,4,6,25,49, causing nephitis invasive rate of about 5%, and nephritis caused by skin infection is mainly type 49, a few For types 2, 55, 57 and 60, the invasive rate is up to 25%.

Low immune system (20%):

The mechanism of glomerular disease is very complicated, and there are many factors involved. The immune mechanism is an important part. The research on immune pathogenesis not only has its theoretical value, but also can guide disease prevention and treatment. It has important clinical significance and bacterial infection. Mostly, the antigen-antibody complex activates complement after glomerular deposition, and induces an inflammatory reaction, while the virus, mycoplasma, etc. directly invade the kidney tissue and cause nephritis. About group A -hemolytic streptococcus infection leads to nephritis The mechanism is generally believed that the body produces antibodies against certain antigenic components of Streptococcus (such as the M protein of the cell wall or certain antigenic components of the cytoplasm), forming a circulating immune complex that reaches the kidney with blood flow and deposits in the kidney. The base membrane of the ball, which activates complement, causes local immunopathological operation of the glomerulus and causes disease. However, other mechanisms have been proposed in recent years. Some people think that certain cationic antigens in Streptococcus are first implanted in the glomerular basement membrane. In situ complex method pathogenicity: The nephrit streptococcus strain changes the normal IgG of the body by secreting neuraminidase, thereby making it antigenic. The antibody is produced and deposited in the kidney. Some people think that the streptococcal antigen and the glomerular basement membrane glycoprotein have cross-antigenicity. This few cases are renal antibody-type nephritis, and the streptococcal antigen deposited in the kidney has not been clear. It is thought to be its cell wall antigen (M protein), but no M protein deposition was found in the glomerulus. It was found that endosfrcptosin, nephritis strain synergistic protein and pre-absorbed antigen were deposited in the patient's glomerulus. Preadsorbing antigen) and other streptococcal components, but whether APSGN is caused by the above-mentioned antigens is not completely confirmed by the immune mechanism.

Pathological changes (25%):

Early renal biopsy of APSGN is mainly diffuse capillary proliferative glomerulonephritis, glomerular enlargement under light microscope, proliferation of endothelial cells and mesangial cells (called intracapillary hyperplasia), neutral polymorphonuclear nucleus Leukocytes and monocytes infiltrate in the glomerulus, narrowing or even occluding the capillary wall, but the capillary wall is usually free of necrosis, along the outer side of the basement membrane of the capillary wall, occasionally with discontinuous proteinaceous deposits (hump), ie The deposited immune complexes showed massive electron-dense deposits on the epithelial side under electron microscopy. In a few glomeruli, localized extravascular hyperplasia (crescent) was observed, but few diffuse crescents were found. Formation, glomerular vessels and tubulointerstitial regions are generally normal, red blood cells are common in the distal small lumen, can form red blood cell casts, immunofluorescence can be divided into mesangial, star-shaped, garland IgG particle-like deposition is observed around the capillary vasospasm and in the mesangial area, often accompanied by C3 and properdin deposition, but less G1q and C4 deposition, changes in serum complement composition, and glomerular capillary vasospasm C3, prepared Pigment deposition, complement activation may indicate that the main way the alternative pathway.

Beta hemolytic streptococcus group A.

Prevention of acute glomerulonephritis in children

The basic prevention is to prevent streptococcal infection. In general, exercise should be strengthened, and the skin should be cleaned and cleaned to reduce respiratory and skin infections. For example, once infected, it should be thoroughly treated in time. After 2 to 3 weeks after infection, urine routine should be checked and abnormalities should be found. . Take a full rest, regardless of the severity of the disease, should stay in bed until the edema significantly subsided, normal blood pressure and gross hematuria disappear, usually takes 2 to 3 weeks. After the erythrocyte sedimentation rate is normal, you can go to school, but you should control the amount of activity.

Complications of acute glomerulonephritis in children Complications hypertensive encephalopathy acute renal failure chronic nephritis

Severe cases of acute severe cases often complicated by severe circulatory congestion, hypertensive encephalopathy and acute renal failure, often resulting in death of children, and very few develop into chronic nephritis.

Acute glomerular nephritis symptoms in children Common symptoms Proteinuria pleural effusion heart sound low blunt hyperkalemia fatigue hematuria metabolic acidosis hypoproteinemia hypertension without urine

1. Typical case:

(1) History of prodromal disease: 10 days before the onset of illness, there are often episodes of infection of streptococcus such as upper respiratory tract infection and tonsillitis. The history of pre-existing disease with skin impetigo is slightly longer, about 2 to 4 weeks.

(2) Edema: It is often the first symptom to appear. It is mainly caused by eyelids and face at the beginning, and gradually descends to the extremities. It is non-depressed, and it is extremely rare to have ascites and pleural effusion.

(3) Urine volume: the amount of urine is reduced parallel to edema, the less urine, the heavier the edema, the oliguria is the daily urine output of school-age children <400ml, preschool children <300ml, infants <200ml or daily urine volume less than 250ml /m2; no urine standard is urine volume <50ml/m2 per day.

(4) hematuria: 50% to 70% of children in the early stage of the disease may have gross hematuria. After 1 to 2 weeks, they will be converted to microscopic hematuria. Most of the mild patients have no gross hematuria. The change of urine is an indispensable clinical manifestation of this disease. .

(5) Hypertension: seen in 70% of cases, the standard of hypertension in different age groups is different: school-age children 17.3/12kPa (130/90mmHg); pre-school children 16/10.7kPa (120/80mmHg); infants 14.7/79.3 kPa (110/70 mmHg) for hypertension, (6) Others: Some patients may have symptoms of low back pain and dysuria. Hypertension is often accompanied by dizziness, headache, nausea, vomiting and anorexia.

2. Serious cases:

In the early stage of the disease (within 1 week), in addition to the above performance, one of the following clinical manifestations may be a serious case:

(1) acute renal insufficiency: manifested as severe oliguria or even no urine, blood creatinine and urea nitrogen increased significantly, serum creatinine 176mol / L (2mg / dl), hyperkalemia and metabolic acidosis, suffering from Children with nausea and vomiting, fatigue, increased breathing, and increased edema.

(2) severe circulation congestion: high sodium retention can cause severe circulatory congestion and heart failure, edema, etc., manifested as obvious edema, persistent oliguria or even no urine, palpitation, shortness of breath, irritability, can not supine, cyanosis, both lungs Voice, heart sound is low and blunt, heart rate increases, galloping and liver progressive increase, (3) hypertensive encephalopathy: blood pressure suddenly rises above 21.3/14.7kPa (160/110mmHg), exceeding the cerebral vascular compensatory contraction function To cause excessive cerebral blood flow and cerebral edema, such as severe headache, frequent vomiting, blurred vision and even blindness, severe unconsciousness, coma, convulsions, etc. 3. Atypical cases (1) Extrarenal symptomatic nephritis: Also known as urinary mildly changed nephritis, although there is a typical history of streptococcal infection, edema, hypertension and serum complement reduction, with or without urinary, but the urine is often no protein, red blood cells and white blood cells, or transient abnormalities .

(2) acute glomerulonephritis manifested as nephrotic syndrome: acute nephritis with obvious proteinuria may have hypoproteinemia, hyperlipidemia and edema, and can be compared with nephritic nephropathy by dynamic observation of urine test and serum complement test. Syndrome differentiation.

Examination of acute glomerulonephritis in children

Urine analysis

There are large individual differences in urine changes, which are generally expressed as:

(1) The amount of urine is small and the proportion is high.

(2) Commonly there are gross hematuria, the appearance of urine is a smoky brown color, often accompanied by red blood cell casts, and red blood cells in urine sediment are deformed.

(3) There are often proteinuria, but the degree is different. Generally, the 24-hour urine protein is 0.2-3.0 g. If the proteinuria is obvious and lasts for a long time, nephrotic syndrome may occur.

(4) There are white blood cells and white blood cell casts in the urine, especially in the early stage.

(5) A variety of tubular urine: in addition to red blood cell cast, white blood cell cast, there are also transparent tube type, granular tube type and transparent tube type.

2. Blood test

(1) Red blood cell count and hemoglobin may be slightly lower, due to: 1 blood volume expansion, blood dilution, 2 with renal failure, erythropoietin reduction leading to renal anemia, 3 hemolytic anemia.

(2) The white blood cell count can be normal or increased, which is related to whether the primary infection is still present.

(3) The erythrocyte sedimentation rate increases rapidly and can return to normal within 1 to 3 months.

3. Blood biochemistry and renal function tests

Glomerular filtration rate (GFR) decreased to varying degrees, but renal plasma flow was still normal, so the filtration fraction was often reduced. Compared with glomerular function, the renal tubular function was relatively good, and the renal concentrating function could be maintained. Clinical common transient azotemia, blood urea nitrogen, creatinine increased slightly, with acute renal insufficiency may appear blood urea nitrogen, creatinine significantly increased, children with unlimited water, may have light Diluted hyponatremia, in addition to sick children may also have hyperkalemia and metabolic acidosis, plasma protein may be slightly decreased due to blood dilution, in the urine protein to reach the level of nephropathy, serum albumin decreased significantly, and With a certain degree of hyperlipidemia.

4. Evidence of streptococcal infection

Bacterial culture of skin lesions or pharyngeal swabs can be performed to detect group A beta-hemolytic streptococcus, or to detect antibodies against streptococcal hemolysin or enzyme in serum. Anti-"O" (ASO) elevation is seen in more than 80% of respiratory infections. Patients with prodromal symptoms and 50% of patients with impetigo as a prodromal symptom usually start to rise 2 to 3 weeks after infection, reach a peak at 3 to 5 weeks, return to normal within half a year, and detect anti-deoxyribonuclease B (anti-DNAase B), anti-Htase and anti-ADPNase, the increase in activity of these enzymes is evidence of streptococcal infection, Anti-Htasc in the skin The positive rate was higher in infection, Anti-ADPNase was higher in respiratory infections, and Anti-ADPNase B was >90% in both infections.

5. Immunological examination

The decrease of serum total complement (CH50) and complement 3 (C3) levels is the key to the diagnosis of acute glomerulonephritis, but the level of decline is not related to the extent of disease and prognosis; serum gamma globulin and immunoglobulin IgG levels are often increased; serum complement 4 (C4) level was normal or slightly decreased, and the decreased serum complement 3 returned to normal within 1 to 2 months, but only a few months returned to normal.

6. Kidney biopsy

Early manifestations of capillary exudation, proliferative inflammation, proliferation of endothelial cells and mesangial cells, a large number of sediments under the epithelium and a camel-like form, followed by mild mesangial hyperplasia, severe patients may have a large number of crescents .

7.ECG

It can be expressed as a low voltage, and the T wave is low and equal.

8.X line

Chest films can be found to have a slight increase in heart shadow; pulmonary edema can be found when severe circulatory congestion occurs.

9. Ultrasound examination

It can be seen that the kidneys are normal or diffusely enlarged, and the cortical echo is enhanced; when severe circulatory congestion occurs, the liver enlarges.

Diagnosis and diagnosis of acute glomerulonephritis in children

Diagnostic criteria

1. Clinical features

Typical acute glomerulonephritis is not difficult to diagnose. After streptococcal infection, edema, hypertension, hematuria (may be associated with varying degrees of proteinuria), and dynamic changes of blood C3 after 1 to 3 weeks of asymptomatic intermittent period. The diagnosis can be confirmed.

2. Laboratory examination

However, the diagnosis of APSGN needs to include 2 of the following 3 points:

(1) Detection of pathogenic bacteria: In the pharyngeal or skin lesions, -hemolytic streptococcus which causes nephritis is detected.

(2) Detection of antibodies: one or more antibodies against Streptococcus components, such as ASO, anti-DNAaseB antibody, anti-Hase antibody, anti-ADPNase antibody, etc., in order to make the diagnostic accuracy reach 90%, A variety of antibody tests must be performed. It is worth noting that early treatment with antibiotics can prevent the production of these antibodies and make the pharyngeal bacteria culture negative, but not prevent the occurrence of APSGN.

(3) Completion reduction: serum complement C3 decreased.

Differential diagnosis

Because many kidney diseases can be manifested as acute nephritis syndrome, and some kidney diseases are associated with a decrease in blood C3, a differential diagnosis is needed.

1. Glomerulonephritis after infection by other pathogens

It is known that a variety of pathogen infections can also cause nephritis, and it is manifested as acute nephritis syndrome. The pathogens that cause proliferative nephritis include bacteria (staphylococcus, pneumococcal, etc.), viruses (influenza virus, Epstein-Barr virus, varicella virus, Kosaki Virus, mumps virus, ECHO virus, giant cell inclusion body virus and hepatitis B virus, etc.), Mycoplasma pneumoniae and protozoa, etc., reference medical history, primary infection and their respective characteristics can be generally distinguished, these patients with nephritis often The decline in C3 is not as significant as APSGN.

2. Other primary glomerular disorders

(1) Membrane proliferative nephritis: onset of acute nephritis, but often significant proteinuria, blood complement C3 continues to be low, the course of the disease is a chronic process, if necessary, renal biopsy identification.

(2) Rapid progressive nephritis: the onset is the same as acute nephritis. The disease progresses continuously in 3 months, hematuria, hypertension, acute renal failure with oliguria persists, and the mortality rate is high.

(3) IgA nephropathy: more than 1 to 2 days after the upper respiratory tract infection, hemorrhagic disease, usually without edema and high blood pressure, generally no serum complement decreased, sometimes there are multiple history of hematuria, when identification is difficult Kidney biopsy.

(4) primary nephrotic syndrome nephritis type: nephritis in the acute phase occasional proteinuria severely reached the level of nephropathy, and is easily confused with nephritic nephrotic syndrome, after analysis of medical history, complement detection, and even after a stage of follow-up observation, can be distinguished Kidney biopsy is required when it is difficult.

3. Secondary kidney disease

Can also be acute onset of nephritis syndrome, such as systemic lupus erythematosus, allergic purpura, hemolytic uremic syndrome, necrotizing small vasculitis, Goodpasture syndrome, according to other manifestations of various diseases can be identified.

4. Acute urinary tract infection or pyelonephritis

In children, hemorrhea can also be manifested, but there are many fevers, urinary tract irritation, white blood cells in the urine, urine culture can be positive.

5. Acute exacerbation of chronic nephritis

Childhood cases are rare, often have a history of previous kidney disease, seizures often induced 1 to 2 days after infection, lack of intermittent period, and often have heavier anemia, persistent hypertension, renal insufficiency, sometimes accompanied by heart, fundus changes, urine specific gravity Fixed, B-ultrasound sometimes sees two kidneys smaller.

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