acute glomerulonephritis
Introduction
Introduction to acute glomerulonephritis Acute glomerulonephritis (acuteglomerulonephritis), that is, acute postinfectious glomerulonephritis (acutepostinfectiousglomerulonephritis), often referred to as acute nephritis. Broadly refers to a group of etiology and pathogenesis, but clinical manifestations of acute onset, glomerular disease characterized by hematuria, proteinuria, edema, hypertension and decreased glomerular filtration rate, therefore Often called acute nephritis syndrome (acutenephriticsyndrome). The vast majority of clinically belong to glomerulonephritis (acutepoststreptococcalglomerulone phritis) after acute streptococcal infection. This disease is the most common kidney disease in childhood. The age is more common in 3 to 8 years old, and rare under 2 years old. The ratio of male to female is about 2:1. Acute glomerulonephritis often occurs after infection. The most common pathogen is beta-hemolytic streptococcus, occasionally in staphylococcus, pneumococcus, typhoid bacillus, diphtheria and protozoa such as malaria parasite, schistosomiasis and virus, clinical Glomerulonephritis is most common after infection with acute streptococcal disease. AGN is common in the pharynx or skin group A after 1-3 weeks of infection with streptococcus hemolytic streptococcus, rarely secondary to other infections (such as staphylococcus, pneumococci) , Group C Streptococcus, virus or parasite). basic knowledge Sickness ratio: 1-3% Susceptible people: more common in 3 to 8 years old Mode of infection: non-infectious Complications: pulmonary edema heart failure cough liver enlargement hypertension coma optic disc edema acute renal failure hematuria hyperkalemia metabolic acidosis uremia
Cause
Causes of acute glomerulonephritis
(1) Causes of the disease
Acute glomerulonephritis often occurs after infection. The most common pathogen is beta-hemolytic streptococcus, occasionally in staphylococcus, pneumococcus, typhoid bacillus, diphtheria and protozoa such as malaria parasite, schistosomiasis and virus, clinical Glomerulonephritis is most common after infection with acute streptococcal disease. AGN is common in the pharynx or skin group A after 1-3 weeks of infection with streptococcus hemolytic streptococcus, rarely secondary to other infections (such as staphylococcus, pneumococci) , Group C Streptococcus, virus or parasite).
(two) pathogenesis
The exact pathogenesis of AGN is unclear. It is known to be an immune complex disease in the acute phase, and is marked by antibody formation against streptococcal antigens and complement immune complex covering the kidney. AGN only occurs in group A -hemolytic streptococcus infection. After the latter, the latter is called a nephritis strain, and the typical nephritogenic strain antibody is directed against its cell wall antigen M type 1, 2, 4, 12, 18, 25, 49, 55, 57, 60, AGN is considered to be mediated by immunity. The immune complex disease has three evidences: 1 The incubation period after the infection with Streptococcus mutans is equivalent to the time when the body is immune after the first infection; 2 The early cycle immune complex is positive, the serum complement is decreased; 3 The immunofluorescence IgG, C3 is granule The deposition in the glomerular mesangial area and capillary vasospasm, but the mechanism of how to cause progressive renal damage and ultimately glomerular sclerosis is not clear.
Studies have shown that all types of proliferative glomerulonephritis have significant glomerular and interstitial inflammatory cell infiltration, while non-proliferative glomerulonephritis has only a small amount of inflammatory cell aggregation in proliferative glomeruli In nephritis, mononuclear cells and T lymphocyte infiltration in the glomeruli are significantly increased, which is related to the severity of proteinuria.
Glomerular immune deposits activate the complement system, which is mediated by inflammatory cells and is involved in the immune response that causes nephritis, and the pathogenic properties of the complement system clearly also contain cell-independent mechanisms, such as C3a, The production of C5a and anaphylatoxins leads to the release of histamine, resulting in increased capillary permeability, and the terminal component of complement C5b-C9 complex (membrane attack complex) has a direct effect on the glomerular capillary basement membrane, C3a - The non-dissolving effect of the C5a component stimulates platelet secretion of serotonin (serotonin) and thromboxane B; stimulates macrophage secretion of phospholipids and arachidonic acid; stimulates mesangial cells to secrete prostaglandins, proteolytic enzymes, phospholipases and Oxygen free radicals and the like constitute inflammatory mediators, and these inflammatory mediators can cause inflammatory lesions of the glomeruli.
Recent evidence supports the notion that one or more streptococcal antigens that have affinity for the glomerular structure are implanted in the glomerulus early in the streptococcal infection, followed by antibody antibodies produced by the host immune response 10 to 14 days later. Antigen binding leads to the development of diseases. The most likely candidate antigens include: Streptococcus nephropathy-associated protein (which inhibits streptokinase activity) and nephritis-binding protein (precursor of pyrogenic exotoxin B), although circulating immune complexes The concentration is not related to the severity of the disease, but it may play a role in the formation of the original in situ immune complex, the development of a large number of glomerular immunoprecipitations, and the alteration of the glomerular basement membrane permeability.
Prevention
Acute glomerulonephritis prevention
Active prevention of streptococcal infection can significantly reduce the incidence of this disease. It should be well insulated to prevent scarlet fever and purulent tonsillitis; keep skin clean and prevent impetigo. Once streptococcal infection occurs, effective antibiotic should be given early. Treatment, clinically adequate penicillin treatment, can prevent the prevalence of nephritis strains, and has a significant preventive effect on reducing the incidence of nephritis.
Complication
Acute glomerulonephritis complications Complications pulmonary edema heart failure cough liver hypertensive coma optic disc edema acute renal failure hematuria hyperkalemia metabolic acidosis uremia
1. Severe circulatory congestion and heart failure: due to water and sodium retention, clinical signs of excessive water overload, such as severe edema, circulatory congestion, heart failure, until pulmonary edema, mainly as shortness of breath, can not be supine, chest tightness and Cough, wet bottom of the lungs, enlarged heart, liver, heart rate, gallop, etc., early signs of circulatory congestion, generally with a diuretic effect within 1 to 2 weeks.
2. Hypertensive encephalopathy: the domestic reported incidence rate of 5% to 10%, the general blood pressure is more than 18.7/12kPa, accompanied by visual acuity, convulsions, coma, one of the three symptoms can be diagnosed, often manifested as severe dizziness, vomiting , lethargy, unconsciousness, black sputum, severe cases of paroxysmal convulsions and coma, fundus examination common retinal arteriolar spasm, bleeding, exudation and optic disc edema.
3. Acute renal failure: the incidence rate is 1% to 2%, manifested as oliguria or no urine, increased blood urea nitrogen, varying degrees of hyperkalemia and metabolic acidosis and other uremic changes.
Symptom
Acute glomerular nephritis symptoms common symptoms dizziness edema no hematuria urinary proteinuria hypertension oliguria anorexia nausea
The clinical manifestations of this disease are disparate in severity. The milder can be "subclinical", that is, there is no specific clinical manifestation except for laboratory abnormalities; severe cases are complicated by hypertensive encephalopathy, severe circulatory congestion and acute renal failure.
1. Pre-infection and intermittent period: Pre-existing diseases are often upper respiratory tract infections caused by streptococcus, such as acute suppurative tonsillitis, pharyngitis, lymphadenitis, scarlet fever, etc., or skin infections, including impetigo, edema. There is an asymptomatic intermittent period from pre-infection to open-door, respiratory infections are caused by about 10 days (6 to 14 days), and skin infections are caused by 20 days (14 to 28 days).
2. Clinical manifestations of typical cases: acute onset after 1 to 3 weeks of asymptomatic intermittent period after streptococcal infection, manifested as edema, hematuria, hypertension and varying degrees of renal function involvement.
Edema is the most common symptom caused by a decrease in glomerular filtration rate due to water and sodium retention. Generally, the edema is not very serious. It only affects the eyelids and face at the beginning, and the morning is heavy. The severe ones spread to the whole body, and a few can be accompanied by chest and ascites. The lighter only gains weight and the body has fullness. The edema pressure of acute nephritis is not concave, and it is different from the obvious concave edema in nephrotic syndrome.
Half of the sick children have meat hematuria; microscopic hematuria is found in almost all cases. In the case of gross hematuria, the urine color can be washed water, smoked gray, brownish red or bright red. The difference in color of hematuria is related to the pH of urine; acidic urine is ash or brownish red, and neutral or alkaline urine is bright red or washed meat. When the gross hematuria is severe, it may be accompanied by dysuria or difficulty urinating. Usually, gross hematuria changes to microscopic hematuria after 1 to 2 weeks, and a few last for 3 to 4 weeks. It can also be temporarily repeated due to infection and fatigue. Microscopic hematuria lasts for 1 to 3 months, and a few last for half a year or more, but the vast majority can be recovered. Hematuria is often accompanied by proteinuria of varying degrees, usually mild to moderate, and a few can reach kidney disease levels. It is not uncommon to reduce the amount of urine, but there are only a few who have at least urine or no urine in the hall.
Hypertension is seen in 30% to 80% of cases, which is caused by the expansion of blood and sodium retention, generally mild or moderate. After more than 1 to 2 weeks, the blood pressure drops to normal with diuretic swelling, and if it does not fall, the possibility of acute exacerbation of chronic nephritis should be considered.
At the same time as the above symptoms, the child often has fatigue, nausea, vomiting, dizziness, the elderly complained of dull pain in the waist, and the young child complained of abdominal pain.
3. Typical morning case performance: There are the following types:
(1) Asymptomatic subclinical cases, which can be completely edema, high blood pressure, gross hematuria, only when the streptococcal infection is prevalent, or in the close contact of children with acute nephritis, microscopic examination is found, and microscopic hematuria is found. The urine test was normal, and only the complement C3 in the blood was reduced, and it recovered after 6-8 weeks.
(2) clinical manifestations of edema, hypertension, or even severe circulatory congestion and hypertensive encephalopathy, and urinary changes or normal routine examination, called "extra-renal symptomatic nephritis", such children with acute complement of blood C3 Decline, a typical regular change in recovery from 6 to 8 weeks, which is helpful for diagnosis.
(3) urinary protein and edema are heavy, even similar to nephropathy. Some sick children may also have plasma protein decline and hyperlipidemia, but it is not easy to distinguish from nephrotic syndrome.
Examine
Examination of acute glomerulonephritis
1. Urine routine examination: microscopic examination showed that red blood cells increased significantly, urine sediment examination of red blood cells reached 10 full field of view / high power microscope, also visible granular tube type, red blood cell cast, renal tubular epithelial cells and white blood cells; urine protein, such urine routine Changes often occur for several months, and fibrin degradation products (FDP) can also occur in the urine.
2. Blood test: common positive pigment, positive cell anemia, hemoglobin is generally 100 ~ 120g / L, mainly related to water and sodium retention, blood dilution, and the degree of uremia, white blood cell count is normal or increased, acute erythrocyte sedimentation The period is often increasing.
Renal function tests showed that the glomerular filtration rate (GFR) decreased in the acute phase. Some patients may have obvious azotemia, BUN and Scr in the blood, hyperkalemia, dilute hyponatremia, and high Chloral acidemia, plasma protein decreased, severe cases of oliguria, no urine or acute renal insufficiency, significant azotemia, metabolic acidosis and electrolyte imbalance; but renal tubular function changes slightly.
3. Bacteriology and serological examination: About half of the patients without pharyngeal or skin purulent secretions showed positive for group A hemolytic streptococcus, about 70% of patients, serum anti-streptolysin "O "(ASO) titer >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 of recent streptococcal infection, commonly used anti-streptolysin "O" and "S" (ASO, ASS), anti-streptokinase, hyaluronidase, anti-DNAM enzyme B, in which ASO is widely used in clinical practice, the titer rises (>1:200) 3 weeks after streptococcal infection, reaches a peak in 3 to 5 weeks, and then gradually Decreased, about half of them returned to normal within 6 months. After pyoderma, nephritis serum ASO, anti-DPNase titer was low, and the positive rate of anti-phosphatase (ASH) and anti-DNase was higher.
Complement level measurement showed that the majority of patients with complement C3 and CH50 properdin decreased, C3 <0.8mg / ml, 6-8 weeks after the disease can return to normal, if the complement continues to decline without return to normal, it should be suspected mesangial capillary Vascular nephritis or other systemic diseases (SLE, etc.), partial cases of circulating immune complex (CIC) test positive and cryoglobulinemia, blood fibrinogen, factor VIII and cytoplasmic activity increased.
4. 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 the presence of hypoproteinemia. And hyperlipidemia.
5. Detection of anti-nuclear antibodies, anti-double-stranded DNA antibodies, anti-Sm antibodies, anti-RNP antibodies and anti-histone antibodies to exclude systemic lupus erythematosus.
6. Hepatic function and detection of hepatitis B virus infection markers except hepatitis B nephritis.
7. Abdominal X-ray film shows normal or enlarged kidney shadow.
8. Chest X-rays The heart can be normal or slightly enlarged, often accompanied by pulmonary congestion.
9. Kidney biopsy
(1) Under the light microscope, the glomerulus is enlarged, the cell components are increased, the vasospasm is hypertrophy, the endothelial cells are swollen, the mesangial cells and the mesangial matrix are proliferated, the capillaries are blocked to varying degrees, and often accompanied by exudative inflammation. Visible neutrophil infiltration, due to hyperplasia, the degree of exudation is different, only some mesangial cells proliferate in the light; severe endothelial cells also proliferate, and some or even all block capillary vasospasm; more serious form a crescent The clinical manifestations of the rapid progression are 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), and the hump usually disappears 6-8 weeks after the disease.
(3) Immunofluorescence: diffuse granular IgG, C3, properdin and fibrin-related antigen deposition along the capillary vasospasm and mesangial area, occasionally IgM, IgA, C1q, C4, etc., renal biopsy of the disease The indications are: 1 oliguria for more than 1 week or progressive urine loss with renal function deterioration, there may be rapid progressive nephritis; 2 2 to 3 months after the onset of the disease did not improve, there is still high blood pressure, sustained Low complement syndrome; 3 acute nephritic syndrome with nephrotic syndrome.
Diagnosis
Diagnosis and diagnosis of acute glomerulonephritis
Diagnostic criteria
Acute nephritis with typical clinical symptoms is not difficult to diagnose. The main diagnosis is based on:
1. There is a history of obvious streptococcal infection before the disease: clinical manifestations of hematuria, proteinuria, oliguria, edema, hypertension and other acute nephritis syndrome.
2. Streptococcus culture and serological examination: pharyngeal or skin purulent secretion culture showed positive group A hemolytic streptococcus, serum complement decreased, serum ASO increased, can confirm the diagnosis of the disease, clinical manifestations are not typical, according to Urine examination and serum complement dynamic changes to make a diagnosis, because 90% of acute streptococcal infection after glomerulonephritis have hypo-complementemia, so serum complement determination can be used as a first line test for the evaluation of acute nephritis.
Differential diagnosis
1. Systemic infectious fever disease: When various infections cause fever, renal blood flow and glomerular permeability can be increased, and transient proteinuria can also occur. This change occurs in high fever, early infection, and fever After the urine returned to normal, there are no other symptoms of acute nephritis syndrome.
2. Multiple primary glomerular diseases characterized by acute nephritis syndrome:
(1) Mesangial capillary glomerulonephritis: the onset process is similar to this disease, but low-complementemia lasts for a long time, and the disease has no self-healing tendency. A large amount of proteinuria and persistent hypocomplementemia are the characteristics of this disease. Renal biopsy can clearly identify the diagnosis.
(2) Rapid progressive nephritis: the onset is similar to acute nephritis, but the symptoms are more severe, mostly progressive oliguria, no urine, rapid development of the disease, renal failure soon, kidney biopsy can be diagnosed in time and with the disease Identification.
(3) IgA nephropathy: more than 1 to 3 days after acute upper respiratory tract infection, hematuria, or with proteinuria, normal serum complement, blood IgA levels can be elevated, the disease is easy to recurrent.
3. Chronic glomerulonephritis acute attack: These patients have a history of kidney disease and similar attacks, rapid onset after infection, no incubation period, more with anemia, persistent hypertension and renal insufficiency, B-ultrasound showed two kidneys Zoom out.
4. Systemic diseases: systemic lupus erythematosus nephritis, allergic purpura nephritis can occur acute nephritis syndrome, these two diseases have obvious skin lesions and joint pain and other arthritis symptoms, the former blood lupus cells and anti- The DNA antibody is positive, and the latter beam arm test is positive. As long as the medical history is detailed and relevant examination is performed, a correct diagnosis can be made.
