Primary acute glomerulonephritis

Pathology and pathogenesis of acute glomerulonephritis (acute glomerulonephritis) is immune reaction caused by diffuse glomerular damage, Most of the people are infected with Streptococcus acute nephritis. It was based on the acute onset of hematuria, proteinuria, edema, hypertension or with azotemia short of the major features of a syndrome group, is known as acute nephritis syndrome (acute nephritic syndrome), children and youth styles. Causes have not yet been fully specified. Known certain factors may cause acute glomerulonephritis. One of the most common is beta-hemolytic streptococcus Group A, followed by other bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Salmonella typhi, diphtheria bacilli and viruses, Plasmodium; Another DNA antigen, tumor antigens, thyroglobulin antigen can be induced glomerulonephritis. However, in patients with acute nephritis, no predisposing factors. Most patients with glomerular pathology showed endothelial cells, mesangial cell proliferation acute diffuse, a few exudative lesions, Another small portion was mesangial, capillary lesions (a membrane proliferative lesions), serious proliferation of mesangial glomerulonephritis can be separated into small fronds. Occasionally balloon crescent formation. Electron microscope can be seen on the skin of electron-dense material was deposited Hump, the characteristics of this disease. But the changes disappear quickly, three months after onset is not easy to see that many of these sediments adjacent to the epithelium, sometimes, subcutaneous. Immunofluorescent test, containing immune globulin, mainly IgG, IgM, IgA can see, It also has C3 deposition, a fashion streptococcal antigen can be seen in mesangial area sediments. Pathogenesis of acute glomerulonephritis is not a direct cause of glomerular damage, but as antigen causes as a result of an autoimmune disease. Is a streptococcal infection after acute glomerulonephritis as an example to illustrate my point. When hemolytic streptococcus infection, Streptococcus body as antigens to stimulate the body to produce B-lymphocyte antibodies; slightly more than when antigen antibody formation of soluble immune complexes, and the deposition in the glomerular endothelial below to nephritis. Some people think Streptococcus membrane antigen and glomerular basement membrane antigen between cross-reactivity, Streptococcus membrane that is the corresponding antibody, and glomerular basement membrane can be combined, resulting activation of complement system, luring WBC, platelet release of the first three factors and the formation of oxygen free radicals, which occurred diffuse glomerular inflammation. In addition, some non-immunologic factors involved in the pathogenesis of glomerulonephritis : If ?٠kallikrein enable increased capillary permeability, Protein increased glomerular filtration and urinary protein excretion increased. ?ڠprostaglandin can affect glomerular capillary permeability. ?۠platelet activating factor induced cationic protein in glomerular deposition, promote urinary protein loss, However, the pathogenesis of nephritis is not entirely clear, still need to be further explored. A clinical performance, the precursor symptoms of the disease before 1 -3 more weeks with respiratory or skin infection, such as acute pharyngitis and tonsillitis. gum abscess, scarlet fever, chicken pox, measles, herpes skin abscess, some patients may not prodromal symptoms. 2, hematuria gross hematuria often one of the first symptoms (about 40 -70%), Urine color is deep brown-red or stale meat washing water, generally within a few days away, and sustainable only 1 -2 weeks to microscopic hematuria. microscopic hematuria more than six months away, and continued for 1 to 3 years before disappearing. 3, puffiness and swelling to oliguria as the first symptoms about 70%, more swelling occurred in the face, eyelid. Eyelid and facial swelling and pale, showing the so-called nephritis face. Edema can also affected leg, a serious chest, pericardial effusion and ascites. Oliguria and edema occurred at the same time when the onset much less urine daily urine output of less than 400 ml, with edema and increased urine output and the more reduction, individual patients can anuria. Edema due to the occurrence of renal lesions small ball filtration rate reduction, and tubular water, sodium reabsorption is fairly good (that is, an imbalance of the ball), caused water, sodium accumulation wandering; Another result of increased capillary permeability, Plasma water seepage to the organization gap; renal ischemia, renin secretion through the renin-angiotensin system. may cause sodium and water pond wandering. Most patients with edema can be dissipated condition improves. 4, hypertension blood pressure can be obtained from the mild to moderate increase Adult general for 20 ~ ~ 14.7kpa 21.3/12, with the increased urine, blood pressure tended to normal. 2 -4 generally sustained weeks. Few patients can dramatically increased blood pressure ( "26.7/17.3kpa) where hypertensive encephalopathy, or left ventricular failure, hypertension mainly with water, sodium accumulation fond of renin secretion and prostaglandin secretion reduced. 5, nervous system symptoms of headache, nausea, vomiting, insomnia, thinking retardation; Have severe visual impairment, or even black Mongolian, coma, convulsion, and more hypertension and water, sodium wandering the pond. A laboratory test, urine routine ?٠proteinuria the characteristics of this disease, urinary protein content varying generally a -3g/24h. (urinary protein qualitative +--+++), few weeks after the gradual reduction of urinary protein to sustain a small ~ +, In 2001 more negative or very low. ?ڠRBC form of microscopic hematuria more shrinkage, and the margin was more or the whole shape, because this glomerular capillary wall damage, RBC through glomerular basement membrane fracture deformation occurred, and within the tubular hypertonic environment. RBC tube existence help in the diagnosis of acute glomerulonephritis. In addition, the granular tube, Sau Ming tube and WBC, a relatively small number, no stain. ?۠urine specific gravity, more 1.020 above, the ball is mainly a function of imbalances in the draft. 2, blood hemoglobin can be a transient mild decline, and hemodilution, In no circumstances Tienam WBC and classification of normal. 3, the majority of renal function in patients with no abnormal renal function, but will have a sexual glomerular filtration function, temporary azotemia. Often accompanies increased urine gradually returned to normal. Individual cases because of a serious illness, renal failure and life-threatening. 4, blood electrolyte electrolyte rare disorder, oliguria, the combination of carbon dioxide may be slightly lower mild increase in serum potassium concentration and dilution sexual hyponatremia, this phenomenon started with the diuretic quickly returned to normal. 5, the serum concentration of complement in 80-95% of patients after the onset of two weeks will have total serum complement C3 and lower four weeks after a complex ,6-8 weeks to resume to normal levels. 6, Antistreptolysin "0" suggest a higher history of streptococcal infection, streptococcal infection in 1 -3 weeks after starting to increase 3 items of article number-5 6th value, followed gradually reduced, About 50% of the patients returned to normal within six months. streptococcal infection after acute nephritis 70 -90% Antistreptolysin "O" titer increased. 7, urine fibrin degradation products (Fibrin degradation products, FDP) Determination of urinary FDP reflect renal intravascular coagulation and fibrinolysis role. FDP within normal urine "2 mg / L (2ug/ml), nephritis urinary FDP value increased. 8, the other will have anti-DNA antibodies, hyaluronidase and serum antibody immune complexes positive, the growth rate of ESR. Diagnosis and differential diagnosis of acute glomerulonephritis according to a pioneer of infection, edema, hematuria, accompanied by hypertension and proteinuria, Diagnosis is not difficult. Acute many Antistreptolysin "0" titer increased serum complement levels declined FDP content in urine increased, and so on contribute to the diagnosis. Individual patients with acute congestive heart failure or hypertensive encephalopathy initial symptoms, Only in early disease or edema and hypertension while only little or no change in urine, not to be a typical case in detail about history, System check-binding comprehensive laboratory analysis, in order to avoid misdiagnosis, in the clinical diagnosis difficult, if necessary, before being diagnosed renal biopsy done. Differential diagnosis of a hot proteinuria in acute febrile infection, the patient may appear proteinuria, or urine tube microscopic hematuria. vulnerable with atypical or mild acute glomerulonephritis confused. Heat proteinuria but no latency stage, no edema and hypertension, heat regressive urine quickly returning to normal. 2. chronic glomerulonephritis acute exacerbation of chronic glomerulonephritis often respiratory infection after 2 -4 days acute, and its clinical manifestations and changes in urine and acute glomerulonephritis similar, but there are always those chronic nephritis history, anemia, hypoproteinemia, hyperlipidemia, serum complement concentrations of normal occasional persistent decreased urine volume and the proportion of low volatility. Accordingly differential is not difficult, for some clear cases of acute or chronic glomerulonephritis, In addition to renal biopsy pathological differential diagnosis, clinical course and in accordance with the symptoms, signs and laboratory findings of the dynamic changes to be judged. 3, acute rheumatism acute rheumatism to kidney disease for outstanding performance were called rheumatic nephritis, haematuria rare, often microscopic hematuria and urinary protein to a small amount of blood pressure is not normally high, often with acute rheumatic fever while the other performance antirheumatic treatment of urinary protein markedly improved, However, microscopic hematuria lasted for a long time. 4. Henoch - Schonlein Purpura Nephritis or systemic lupus erythematosus (SLE) nephritis Henoch - Schonlein purpura, or lupus nephritis were there will be acute nephritis syndrome, but there are two more obvious skin, joints change. Henoch - Schonlein purpura arm beam test positive. Lupus erythematosus cells can be found in SLE, anti-DNA antibodies and anti-nuclear factor-positive. SLE is often accompanied by fever, so if asked in detail about the history and selectively comprehensive inspection can be differentiated. Necessary to do differential renal biopsy.