Acute nephritis

Introduction to acute nephritis Acute glomerulonephritis, referred to as acute nephritis, is called acute nephritis syndrome because of different causes. It is a group of acute glomerular non-suppurative inflammatory lesions caused by an immune response after acute infection. Clinically, edema, oliguria, hematuria and hypertension are the main manifestations. Pre-existing diseases such as cold, tonsillitis or skin purulent infection are often seen before the onset of the disease. This disease is the most common kidney disease in childhood. Common in children aged 3-8, rarely seen under 2 years old. The prognosis is generally good, the course of disease is 6 months to 1 year, and only a few patients develop chronic nephritis. A small number of children may have serious symptoms in the first week of the onset, such as hypertensive encephalopathy, renal insufficiency, heart failure, etc., so this disease should be given high priority. The disease is often caused by infection of hemolytic streptococcus "nephritis strain", which is common in streptococcal infections such as upper respiratory tract infections (mostly tonsillitis), scarlet fever, skin infections (mostly impetigo). basic knowledge The proportion of illness: 0.003% Susceptible people: common in children aged 3-8 Mode of infection: non-infectious Complications: congestive heart failure, hypertension, acute renal failure, urinary tract infection, uremia

Cause of acute nephritis

Viral infection (26%):

In recent years, it has been found that viral infection can also lead to acute nephritis, including: infectious hepatitis, mumps, chickenpox, flu, infectious mononucleosis, measles and adenovirus, in addition to nephritis after infection with malaria parasites.

Streptococcal infection (35%):

The disease is often caused by infection of hemolytic streptococcus "nephritis strain", which is common in streptococcal infections such as upper respiratory tract infections (mostly tonsillitis), scarlet fever, skin infections (mostly impetigo).

Bacterial infection (16%):

Bacterial infections can also cause disease, including bacteremia, various viral and parasitic diseases, pneumococci, golden yellow and Staphylococcus epidermidis, Klebsiella, meningococcus, typhoid bacillus, and the like.

In summary, the cause of acute nephritis is mainly streptococcal infection, including tonsillitis, pyoderma and erysipelas, followed by staphylococcal infection, pneumococcal infection and viral infection.

Acute nephritis prevention

1, strengthen exercise, enhance physical fitness, increase resistance, especially in winter to increase respiratory resistance is particularly important.

2. Pay attention to strengthen personal hygiene and reduce the chance of streptococcal infection.

3, if pharyngitis, tonsillitis, cold, scarlet fever and other streptococcal infections have occurred, and immediate treatment is also an important part of prevention of acute nephritis.

4, adjust the life, work and rest.

5, some people with poor resistance, susceptible to upper respiratory tract infection in winter, can prevent the use of Qingrejiedu Chinese medicine.

Acute nephritis complications Complications, congestive heart failure, hypertension, acute renal failure, urinary tract infection, uremia

1, acute congestive heart failure: acute left heart failure in children can become the first symptoms of acute nephritis, if not promptly identified and rescued, it can quickly die, acute nephritis, due to water and sodium retention, systemic edema and increased blood volume, Pulmonary circulatory blood stasis is very common, so in the absence of acute heart failure, patients often have shortness of breath, cough and a little wet sputum at the lungs and other symptoms of pulmonary circulation and blood stasis, because the patient also has respiratory infections, so the presence of pulmonary circulation and blood stasis It is easy to be neglected. On the contrary, this kind of circulating blood stasis phenomenon is mistaken for acute heart failure. Therefore, it is very important to correctly understand the pulmonary blood stasis caused by water and sodium retention or acute nephritis complicated with acute heart failure.

2, hypertensive encephalopathy: the incidence of hypertensive encephalopathy in acute nephritis in the past 5% to 10%, in recent years and acute heart failure, its concomitant rate is significantly lower, and less common than acute heart failure, this may be timely Reasonable treatment related, common symptoms are severe headache and vomiting, followed by visual impairment, confusion, lethargy, and may have paroxysmal convulsions or epileptic seizures. After blood pressure control, the above symptoms quickly improve or disappear, no sequelae.

3, acute renal failure: acute phase of acute nephritis, glomerular mesangial cells and endothelial cells proliferate, capillary stenosis and capillary coagulation, patients' urine output further reduces oliguria or anuria, protein catabolism When the product is largely retained, uremic syndrome can occur in the acute phase.

4, secondary bacterial infection: acute nephritis due to reduced systemic resistance, easy to secondary infection, the most common is lung and urinary tract infection, once secondary infection, it should be actively symptomatic treatment, so as not to cause the original disease to increase.

Acute symptoms of nephritis Common symptoms Hematuria proteinuria high blood pressure pregnancy protein urinary fever high heat dull pain fatigue dizziness edema

The clinical manifestations of acute nephritis vary in severity. The mild type can be subclinical (ie, there is no specific clinical manifestation except for laboratory abnormalities). The clinical symptoms are not obvious. The severe cases are complicated by hypertensive encephalopathy, severe circulatory congestion and acute renal failure. The severity varies greatly. Most patients have a history of pre-infection, the incubation period of upper respiratory tract infection is 1 to 2 weeks, and the incubation period of streptococcal infection is 3 to 4 weeks. Lighter patients have no obvious history of infection, only the anti-streptolysin "O" titer is elevated, and the degree of nephritis does not depend on the severity of the precursor infection. The typical symptoms are acute onset after 1 to 3 weeks of asymptomatic latency after pre-infection, manifested as acute glomerulonephritis syndrome, mainly hematuria, proteinuria, edema, oliguria, hypertension and renal dysfunction.

1, abnormal urine

Almost all patients have glomerular hematuria, and some patients may have gross hematuria, which is often the first symptom of onset and the cause of the patient's visit.

2, edema

Most patients have edema, often the initial onset of onset, typical manifestations of morning eyelid edema or mild concave edema of the lower extremities, a few severe cases can affect the whole body.

3, high blood pressure

Most patients have transient mild to moderate hypertension, often associated with sodium retention, and blood pressure can gradually return to normal after diuresis. A small number of patients may have severe hypertension and even hypertensive encephalopathy.

4, abnormal renal function

The patient's early urine volume decreased (usually 400 ~ 700ml / d), a small number of patients even oliguria (<400ml / d). Renal function can be transiently impaired, manifested as mild azotemia. After more than 1 to 2 weeks, the amount of urine increases gradually, and the renal function gradually returns to normal after several days of diuresis. Only a very small number of patients can present with acute renal failure.

5, congestive heart failure

Often occurring in the acute nephritis syndrome, patients may have jugular vein engorgement, galloping and pulmonary edema symptoms.

6, the whole body performance

Patients often have fatigue, anorexia, nausea, vomiting, dizziness, headache, and occasionally coexist with rheumatic fever. The lightest subclinical patients had only microscopic hematuria, or even urine tests were normal. Only blood C3 showed a regular change, and the acute phase decreased significantly, recovering from 6 to 8 weeks. Renal biopsy has typical pathological changes.

Examination of acute nephritis

Laboratory inspection

1, urine routine

Hematuria is an important finding of acute glomerulonephritis, or gross hematuria or microscopic hematuria. The red blood cells in the urine are mostly severely deformed red blood cells, but when the diuretic is applied, the non-renal deformed red blood cells can be temporarily used. In addition, the red blood cell cast type can be seen, suggesting that the glomerulus has hemorrhagic exudative inflammation, which is an important feature of acute glomerulonephritis. Urine sediment is also common in renal tubular epithelial cells, white blood cells, a large number of transparent and granular casts. Urine protein is usually (+) ~ (++), urine protein is mostly non-selective, and urinary fibrin degradation products (FDP) increase. Urine routines generally return to normal within 4 to 8 weeks. Residual microscopic hematuria (or Abdi count) or small amounts of proteinuria (which can be expressed as standing proteinuria) can last for six months or longer.

2, blood routine

Red blood cell count and hemoglobin may be slightly lower due to blood volume expansion and blood dilution. The white blood cell count can be normal or increased, which is related to whether the primary infection is still present. ESR increased quickly and returned to normal within 2 to 3 months.

3, blood chemistry and renal function tests

Glomerular filtration rate (GFR) decreased to varying degrees, but renal plasma flow was still normal, and the filtration fraction was often reduced. Compared with glomerular function, the renal tubular function is relatively good, and the renal concentrating function can be maintained. Clinical common transient azotemia, blood urea nitrogen, creatinine increased. Children with unlimited water may have mildly diluted hyponatremia. In addition, sick children can also have hyperkalemia and metabolic acidosis. Plasma protein can be slightly decreased due to hemodilution. In patients with proteinuria and nephropathy, albumin is significantly decreased, and may be associated with a certain degree of hyperlipidemia.

4. Bacteriology and serological examination

In patients without antibiotic treatment, approximately half of the pharyngeal or skin purulent secretion cultures showed positive for group A hemolytic streptococcus. In about 70% of patients, the titer of serum anti-streptolysin "O" (ASO) is >400U.

Streptococcus bacteria in vitro antigen components into the human body, can stimulate the body to produce the corresponding antibodies. This antibody can be used as evidence for recent streptococcal infections. Anti-streptolysin "O" and "S" (ASO, ASS), anti-streptokinase, hyaluronidase, and anti-DNAM enzyme B are commonly used. Among them, ASO is widely used in clinical practice. The titer increased (>1:200) 3 weeks after streptococcal infection, reached a peak at 3 to 5 weeks, and then gradually decreased, and about half of the patients returned to normal within 6 months. After pyoderma, the serum ASO and anti-DPNase titers were low, and the positive rates of anti-phosphatidase (ASH) and anti-DNase were higher.

5, blood complement determination

Complement level measurement showed that the majority of patients with complement C3 and CH50 properdin decreased, C3 <0.8mg / ml, more than 6 to 8 weeks after the disease can return to normal. If complement continues to decline without returning to normal, it should be suspected to be mesangial capillary nephritis or other systemic disease (SLE, etc.). In some cases, the circulating immune complex (CIC) test was positive and cryoglobulinemia. Blood fibrinogen, factor VIII and cytoplasmic activity are increased.

6, blood biochemical examination

For patients with severe edema and massive proteinuria, plasma total protein, albumin/globulin ratio, blood cholesterol, triglyceride, and lipoprotein should be measured to determine if hypoproteinemia and hyperlipidemia are present.

7, antibody inspection

Antinuclear antibodies, anti-double-stranded DNA antibodies, anti-Sm antibodies, anti-RNP antibodies, and anti-histone antibodies are detected to exclude systemic lupus erythematosus.

8. Detection of liver function and hepatitis B virus infection markers

Hepatic function and hepatitis B virus infection markers were detected except for hepatitis B nephritis.

Auxiliary inspection

1, abdominal X-ray film

Abdominal X-ray plain film shows normal or enlarged kidney shadow.

2, chest X-ray photos

The heart can be normal or slightly enlarged, often accompanied by pulmonary congestion.

3, kidney biopsy

(1) Under the light microscope, the glomerulus is enlarged, the cell components are increased, the vasospasm is hypertrophied, the endothelial cells are swollen, the mesangial cells and mesangial matrix are proliferated, and the capillaries have different degrees of obstruction. In addition, exudative inflammation is often accompanied by neutrophil infiltration. Due to the degree of hyperplasia and exudation, only some mesangial cells proliferate in the light; the endothelial cells also proliferate in the severe cases, and some or even all of the capillary vasospasm can be blocked; more severely, the crescent is formed. Patients with clinical manifestations of acute progression have extensive crescent formation.

(2) Electron microscopy: The typical hump change of the disease can be seen under the epithelium (ie, the deposition of fine dense electrons under the epithelium). Humps generally disappear 6 to 8 weeks after the disease.

(3) Immunofluorescence: diffuse granular IgG, C3, properdin and fibrin-related antigen deposition can be seen along the capillary vasospasm and mesangial area, occasionally IgM, IgA, C1q, C4 and so on. The indications for renal biopsy of this disease are: 1 oliguria for more than 1 week or progressive urine output with renal function deterioration, and may have rapid progressive nephritis; 2 after 2 to 3 months after onset, the condition is not improved, there is still high Blood pressure, persistent hypocomplementemia; 3 acute glomerulonephritis syndrome with nephrotic syndrome.

Diagnosis and diagnosis of acute nephritis

Diagnose based on:

1, there are pre-infections 1-4 weeks before the disease.

2, clinical manifestations of non-depressed edema, oliguria, hematuria, high blood pressure four major symptoms.

3, urine examination has protein, red blood cells and tube type.

4. Serum urea nitrogen increased and creatinine clearance decreased.

Differential diagnosis:

Should be differentiated from acute thermal proteinuria, acute nephritis, lupus nephritis, allergic purpuric nephritis, chronic nephritis (acute episodes), acute allergic interstitial nephritis and other diseases.

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