acute post-infectious nephritis in the elderly
Introduction
Introduction to acute inflammation of the elderly after nephritis Glomerulonephritis, also known as acute nephritis syndrome, is a group of diseases caused by many causes. The common clinical manifestations are acute onset, almost all hematuria, proteinuria, edema and hypertension, which may be accompanied by oliguria and azotemia. The common pathogens are bacteria (staphylococcus, pneumococcal) viruses, protozoa, Spirulina (syphilis), as well as mycoplasma, fungi, etc., the most common in the elderly is acute glomerulonephritis caused by streptococcal infection, skin infection is more common in young people. basic knowledge The proportion of illness: 0.001% Susceptible people: the elderly Mode of infection: non-infectious Complications: congestive heart failure, hypertensive encephalopathy, headache, coma
Cause
Causes of nephritis after acute infection in the elderly
the reason
In the 19th century, acute nephritis was observed to be associated with certain streptococcal infections, but it was later confirmed that not all streptococcal infections can cause acute nephritis, and only the nephritis-producing strains have this pathogenic effect. Mainly in the beta-hemolytic streptococcus group A, mainly type 12, including 1,2,3,4,18,25,49,55,57 and 60, etc., occasionally beta-hemolytic streptococcus group C or Group G infection can also cause disease. The pro-infections caused by these nephritis-producing strains are mainly upper respiratory tract infections (such as pharyngitis or tonsillitis), but skin infections (such as impetigo, often caused by group A type 49) are also very Common, the pathogenic antigen that causes the body's immune response is which component of streptococcus, which is not fully understood. It has long been considered as the M protein of the streptococcal cell wall, but it was later confirmed that this antigen component mainly exists in the cell membrane or cell body, such as Endostreptosin in the cell membrane and nephritic strain associated protein in the cell body. In addition, it is reported that a positively charged antigen in the extracellular component of Streptococcus may also cause disease.
Pathogenesis
Pathogenesis
(1) The disease belongs to immune complex type nephritis. Irregular granule deposits (containing IgG, C3, properdin and trace C1q and C4) can be found on the glomerulus by immunofluorescence. It can be seen that this immune complex is deposited in a hump-like manner outside the basement membrane, and the immunological complex is confirmed by histologically.
The antigen (a component of Streptococcus) and the antibody (immunoglobulin) form an immune complex. In the acute phase of the disease, the immune complex (CIC) in the blood circulation is often measured, and the amount of antigen and antibody is close to equilibrium, and the amount of antigen is When there is a slight excess, a moderately soluble immune complex is formed, which is retained and deposited when passing through the glomerular basement membrane. Others believe that the streptococcal antigen component can bind to fibrinogen in the blood to form a larger molecular weight. The soluble complex, deposited in the mesangial area, causes the cellular inflammatory response.
Certain positively charged components of streptococcal antigens can form "planting antigens" by a charge reaction combined with glomerular structures; MSAP can be "planted" by binding to the glomerular upper chain kinase C receptor; ESS (P15.7-5.9) may be combined with a glycoprotein on GBM by a mechanism similar to phytohemagglutinin, which can lead to the formation of in situ immune complexes.
(2) The role of autoimmune in the pathogenesis of acute nephritis: This possibility has been concerned, but there is no strong evidence. It has been reported that in 2 patients with acute nephritis with typical clinical and pathological diagnosis of this disease, serum was found. DNA and anti-DNA (single-stranded and double-stranded) immune complexes, and anti-DNA antibody titers increased, and reported streptococcal neuraminidase activity and free neuraminic in patients with this disease The elevated level of acid, ie free sialic acid, indicates that the neuraminidase of Streptococcus mutans releases sialic acid from blood immunoglobulins or tissues (including glomeruli), resulting in autoimmunity or normalization. The antigenic determinant of IgG is exposed to form an antibody against autologous IgG (Fig. 1).
(3) Hypocomplementemia: As early as 1914, Gunn had found 4 cases of acute, nephritis patients with hypocomplementemia. In 1935, Kellett further pointed out that hypocomplementemia in acute nephritis is the result of antigen and antibody reaction; Streptococcus in vitro toxins can activate complement directly through the alternative pathway; NSAP activates fibrinogen in the glomerular bloodstream to form fibrin, which activates complement through the alternative pathway, causing an inflammatory process.
After the onset of acute nephritis, CH50, C3 and C5 in the blood decreased significantly, and returned to normal in 6-8 weeks; C1q and C4 decreased slightly, the degree of decline was lighter than C3, and soon returned to normal; B factor was normal; blood The level of phlegm was significantly and persistently decreased, and the recovery was slower than that of C3. Immunofluorescence technique was used to confirm that there was a large amount of C3 and properdin deposition on the glomerulus of patients with acute nephritis. Therefore, most authors believe that the complement of this disease is mainly The alternative pathway is activated, called "alternative pathway disease", but it is also believed that both activation pathways may exist in different patients. The serum of this patient contains substances that activate and consume complement, causing low In complementation, studies have confirmed that C3NeF is an antibody to C3 convertase and is therefore involved in the activation of the complement bypass pathway activation of this disease.
Activation of the complement system causes a series of immunopathological changes, especially the C5b-9 (membrane attack complex) formed by the subcutaneous immune complex to activate complement, which plays an important role in the pathogenesis of acute nephritis.
(4) Immune-mediated inflammatory response: immune complexes, especially those that are deposited in the subendothelial and mesangial regions, which are close to the circulating cells, can attract circulating inflammation through immune and chemical mechanisms. Cells (neutrophils, monocytes), these inflammatory cells and diseased glomerular cells can produce a series of inflammatory mediators, such as cytokines, proteases and activated oxidative metabolites, causing glomerular inflammation, 1 time The immune complex formed by the infection of the streptococci strains, the glomerulus still has the ability to clear (mainly through mesangial cell phagocytosis), interrupting the vicious circle of the above-mentioned immune-inflammation, making the acute nephritis lesion self-limiting.
2. Pathological changes
The gross specimen showed that the bilateral kidneys were swollen up to twice as large as normal people, smooth but grayish white, so it was called large white kidney, the surface was scattered at the bleeding point, the cut surface cortex and medulla were clear, and the cone was congested.
Due to the severity of clinical manifestations and different stages of disease, the corresponding histological changes are also different. Typical cases are diffuse capillary proliferative or mesangial proliferative changes, a few membrane hyperplasia changes, and small kidneys within 1 month of onset The endothelial cells of the ball, the mesangial cells are significantly proliferated or swollen, filled in the small cystic cavity, causing the capillary lumen to be narrow or even occluded, accompanied by multinucleated leukocyte infiltration, so it is also called exudative glomerulonephritis, accompanied by lymphocytes. And CD4+ lymphocytes exist, glomerular basement membrane, renal tubules are normal, but there are multinuclear, mononuclear and T lymphocyte infiltration in the stroma, which has been paid attention to in recent years, and proved to be related to the decline of GFR, mesangial area and basement membrane There are immune deposits, C3, C4 are granular deposits, and properdin is present. Membrane attack complex (C5b-C9) is also localized by granular deposition in the mesangial area. In addition, there are IgG and IgM deposition, in which subepithelial-like deposits are representative.
Immunofluorescence showed that IgG, IgM, and C3 were granulated around the glomerular capillaries, and were classified according to their morphology:
1 star type: 30%, more than 2 weeks after onset, characterized by IgG, C3 along the glomerular capillaries and mesangial diffuse irregular particle deposition, between or with larger capillaries Deposition.
2 mesangial type: 45%, mostly appeared 3 to 6 weeks after onset, IgG, C3 mainly deposited in the glomerular mesangial area of the axis and pedicle, most of the disease has a good prognosis.
3 contains ring type: 25%, IgG, C3 is densely deposited around the capillary, forming a flower ring, while the mesangial deposition is very small, endothelial cells, mesangial cells are obviously proliferating, some capillary wall thickening, often The glomerulus is lobulated, and there is often severe proteinuria in the clinic, and the long-term prognosis is very poor.
Kidney puncture
Histological examination indication: Nephritis is a self-limiting disease after acute streptococcal infection, usually the clinical symptoms can disappear completely in a short period of time, but the microscopic hematuria and/or proteinuria can last for several months, most of the prognosis is good, generally not Kidney puncture is required. The following are indications for renal biopsy to provide diagnosis and guidance treatment:
1 In the acute phase, serum complement or hospital admission decreased, but its value continued to decrease after 2 months. It can be identified by renal biopsy and lupus nephritis or membrane proliferative nephritis.
2 patients with persistent hypertension and massive proteinuria after 3 to 4 weeks of onset.
3 aggravation of azotemia, accompanied by persistent hypertension, suggesting rapid disease development, increased renal damage, kidney biopsy to confirm crescentic nephritis.
3. Pathophysiological changes
(1) Pathophysiological changes in the kidney: The pathophysiological changes in the kidney during acute nephritis are related to the glomerular capillary inflammatory response caused by immune mediated.
1 The glomerular basement membrane is damaged by neutrophils and vasoactive substances and membrane attack complexes (even under the electron microscope), causing intravascular plasma proteins and red blood cells, white blood cells, etc. to escape into the urine, and urine protein formation Another cause is the reduction of phleboplasty and serotonin glycosaminoglycans in the glomerular capillaries, and the destruction of the membrane's negative charge barrier.
2 glomerular capillary vasospasm, glomerular filtration area decreased, resulting in decreased glomerular filtration rate, oliguria and anuria, and even azotemia and uremia.
3 application of aminopurine acid (PAH) clearance rate study of renal blood flow confirmed that acute renal nephritis renal blood flow is normal, and even increased (due to the decline in the arteriolar resistance), therefore, unlike chronic nephritis, the disease is not in the kidney In the ischemic state, the glomerular filtration rate decreases due to normal renal blood flow, and the patient's filtration fraction decreases.
4 The maximum reabsorption function (TmG) of the renal tubules is only mildly impaired or normal, the degree of glomerular filtration rate is more than the degree of tubular damage, the amount of filtered primary urine is reduced, and the time of passage through the renal tubules is prolonged; In addition, after the glomerular capillary vasospasm is blocked, the capillary pressure around the renal tubules decreases. These two factors promote the renal tubular epithelium with less severe functional damage to fully reabsorb the water and sodium in the original urine, causing oliguria. And water, sodium retention, renal sodium excretion fraction is less than 1%, which is the "ball tube imbalance state."
5 Due to the expansion of circulating blood volume, reflex caused plasma renin activity and angiotensin, aldosterone concentration decreased, and the disease recovery period returned to normal; the levels of prostaglandins PGE2, PGF2 and kallikrein in urine continued to decrease.
(2) systemic pathophysiological changes: the central link is sodium and water retention, blood volume expansion, which causes hypertension and edema, severe cases can cause severe complications such as hypertensive encephalopathy and heart failure, is the main cause of death of acute nephritis Therefore, in the treatment of acute nephritis, the blood volume is controlled, and the water retained in the body is excluded, and sodium is the key.
Prevention
Nephritis prevention after acute infection in the elderly
Primary prevention
(1) Enhance the body's ability to resist Streptococcus infection, exercise properly, strengthen nutrition, and try to avoid patients who are exposed to influenza in public places during the winter and spring.
(2) Strengthen health publicity and education to avoid upper respiratory tract and skin infections. Active treatment should be given to those with existing streptococcal infections, and actively treat various chronic diseases such as tonsillitis, sinusitis, dental caries and otitis media.
(3) Strengthen the study of HLA related to the disease and the relatives of the patients, in order to further clarify the relationship between the disease and the disease.
2. Secondary prevention
(1) In the early stage of the original glomerulonephritis, timely treatment should be carried out, and the routine urine test should be carried out in time to prevent the disease from prolonging and causing chronic kidney changes.
(2) For patients with hypertension and anemia, urine routine and renal function tests should be performed to avoid missed diagnosis of chronic nephritis.
(3) If you have the condition, you can take a kidney biopsy as soon as possible to use the drug correctly.
3. Three levels of prevention
The purpose is to delay the deterioration of renal function, and the measures taken are:
(1) Low protein diet.
(2) Control blood pressure.
(3) Prevention of tubulointerstitial damage.
(4) Do not use drugs that are harmful to the kidneys.
Complication
Nephritis complications after acute infection in the elderly Complications, congestive heart failure, hypertensive encephalopathy, headache, coma
1. Circulatory congestion and acute congestive heart failure
The onset is rapid and dangerous. It occurs on average 3 to 5 days after onset. It is easily misdiagnosed as pneumonia complicated with heart failure. In recent years, the mechanism and clinical manifestations of this complication have been recognized. Early diagnosis and timely prognosis are highly optimistic, over 60 years old. The elderly with this disease can reach 43%, the pathogenesis is due to the high blood volume caused by sodium and water retention, resulting in circulatory congestion, many factors causing sodium retention, and the activity of renin-angiotensin-aldosterone system is increased. Important factors also provide an important theoretical basis for the treatment of heart failure with angiotensin-converting enzyme inhibitors. In addition, acute stage edema, urinary plasma levels of plasma natriuretic peptides increase significantly, and its dynamic changes consistent with changes in blood volume is another Key factor.
Clinical manifestations in addition to irritability, cyanosis, edema, oliguria and the following symptoms:
1 pulmonary congestion symptoms: shortness of breath, cough, sitting breathing, pink foam sputum, wet lung sounds on both lungs, chest radiograph showing enlarged heart, enlarged hilar shadows on both sides, increased lung lines, and pleural reaction.
2 heart: heart rate increases, even galloping, apnoea audible and systolic murmur, occasional arrhythmia, severe systolic blood pressure can be reduced. 3 liver enlargement, jugular vein engorgement, increased venous pressure.
2. Hypertensive encephalopathy
In recent years, due to timely and reasonable treatment, the acute chain-like nephritis has been significantly reduced, the incidence rate is about 0.5%. Although hypertension and the disease often exist simultaneously, its role in this disease has not been confirmed, from pathology. From the point of view, most small thrombosis (caused by vasospasm) and cerebral edema can occur in the brain, and there are also cerebral hemorrhage. Cerebral vasospasm and sodium retention are related to cerebral edema, usually dizziness, headache, vomiting, and unconsciousness. Qing, black Mongolian, severe cases of paroxysmal convulsions, coma, when high blood pressure with visual impairment, convulsions, coma, one of the three items can be diagnosed.
Nephritis in elderly patients with acute streptococcal infection is significantly less than that of children, but it is not uncommon. It is difficult to diagnose due to atypical clinical manifestations. Streptococcus pre-existing infection is not typical. Pre-existing skin infection is higher than pharynx, oliguria, difficulty breathing, pulmonary congestion. A large number of proteinuria, azotemia and early mortality of the disease were in the middle and old age. In the 1960s, 46% of the deaths were reported to be 60 years old or older, and 9 cases were reported in 7 cases over 60 years old. He died of acute renal failure, but since the dialysis treatment, the acute renal failure of the elderly patients has been found to be life-long after dialysis. Although the recovery of renal function is slower than that of young people, most patients can still recover completely. Therefore, the total prognosis is no better. Young patients are poor, in addition, the incidence of pulmonary congestion and dyspnea in elderly patients is also significantly higher than that of young people.
Symptom
Symptoms of nephritis after acute infection in the elderly Common symptoms Frequent urination fatigue nausea glomerular filtration rate decreased urine protein dull pain proteinuria with hypertension hematuria drowsiness
Incubation period
Most patients have a history of pre-infection (pharyngeal or cutaneous). The milder can be clinically manifested without infection. Only the anti-streptolysin "0" titer rises. The severity of nephritis does not depend on the severity of the pre-infection.
Clinical symptoms begin to appear 7 to 20 days after streptococcal infection. At this time, most of the clinical manifestations of the primary infection have disappeared, and the incubation period may be shorter. About 1/5 cases are 4 to 7 days, more than 3 to 4 weeks. Very rare, but skin infections have a longer incubation period, averaging 18 to 21 days.
In the process of streptococcal infection, there may also be transient mild proteinuria and microscopic hematuria, which is a urine change in general febrile diseases, or related to the action of erythrogenic toxin on the glomerular basement membrane. However, these patients often have acute nephritis, so it may also be the initial manifestation of nephritis.
2. General performance
The clinical manifestations of this disease range from subclinical to mild to acute renal failure, and the severity varies greatly.
(1) hematuria: often the first symptom of onset, almost all patients have hematuria, of which the gross hematuria rate is about 40%, the urine color is evenly brown turbid or washed meat, but no blood clots, The erythrocyte lysis in acidic urine often causes the urine to be soy-like brown. It disappears in a few days to 1-2 weeks. The urinary tract has discomfort and urinary frequency when the patients with severe hematuria urinate. The microscopic hematuria disappears within half a year. The 3 years disappeared.
(2) proteinuria: almost all patients with urinary protein positive (conventional qualitative method), proteinuria is generally not heavy, 0.5 ~ 3.5g / d, often non-selective proteinuria, only about 20% of patients with urine protein Above 3.5g/d, urine FDP is often increased at this time, and some patients have a very small amount of urinary protein when they visit the clinic, so there is no urine protein positive record.
(3) edema: also often early symptoms of onset, the incidence rate of 70% to 90%, this is a significant reduction in glomerular filtration rate, the main manifestations of the disease accounted for more than 60%, the light is early eyelid edema It is called "nephritic face". When it is severe, it can be extended to the whole body. The finger pressure can be concave. The body weight can be increased by more than 5kg before the disease, and the chest and abdomen effusion appears. Most patients are in 2 to 4 weeks. Self-diuresis, swelling, such as edema or persistent development of nephrotic syndrome often indicates poor prognosis.
Edema is mainly due to the decrease of glomerular filtration rate, and the absorption capacity of renal tubules, especially distal convoluted tubules, and the imbalance of bulb function. Systemic capillary lesions cause increased capillary permeability, hypoproteinemia and heart failure. Other factors can aggravate edema. At present, due to the restriction of salt and diuresis for patients, the degree of edema is generally mild.
(4) Hypertension: seen in about 80% of cases, the elderly are more common, mostly moderate blood pressure, even severe hypertension, increased diastolic blood pressure accounted for more than 80%, but less than 50% of patients exceeded 16kPa (120mmHg), often without hypertensive fundus changes.
The cause of hypertension is mainly related to water and sodium retention, blood volume expansion, plasma renin level is generally not elevated, aldosterone secretion rate is normal or decreased, so the degree of hypertension and edema often parallel, and return to normal with diuresis If the blood pressure continues to rise for more than 2 weeks, there is no downward trend, indicating that the kidney disease is more serious, and persistent hypertension also aggravates renal damage and should be treated early.
(5) oliguria: Most patients have less than 500ml/d of urine when they are on the disease. Nitrogenemia can be caused by oliguria. After 2 weeks, the urine volume is gradually increased and renal function is restored. Only a small number of patients (less than 5%) are Oliguria develops into anuria, indicating severe renal parenchymal lesions.
(6) renal dysfunction: often transient azotemia, mild increase in serum creatinine and urea nitrogen, more severe (crear creatinine > 352mol / L (4.0mg / dl), urea nitrogen > 21.4mmol / L (60mg/dl) should be alert to acute renal failure. After a few days of diuresis, azotemia can return to normal. A small number of elderly patients can not recover after diuresis, and the prognosis is not good.
The glomerular filtration function is transiently damaged, and the renal blood flow is normal, so the renal filtration fraction is correspondingly reduced. This is a typical change of acute nephritis. The involvement of renal tubular function is lighter, and the renal tubular maximum reabsorption of glucose (TmG) ) and renal tubules have a slight decrease or normalization of PAH maximum excretion (Tm PAH), urinary sodium and urinary calcium decreased, sodium excretion fraction is less than 1%, renal failure index is less than 1, and urine concentration function is normal.
(7) systemic manifestations: patients often have fatigue, anorexia, nausea, vomiting (not completely proportional to azotemia), lethargy, dizziness, blurred vision (related to high blood pressure and cerebral ischemia, cerebral edema) and waist Dull pain (due to the enlargement of the renal parenchyma, bulging the kidney capsule, involving the sensory nerve endings).
3. Other clinical types
Typical cases have obvious clinical manifestations and are easy to diagnose, but there are several clinical types, and their clinical manifestations, pathological changes and treatment responses are different:
(1) Light (subclinical): only mild urinary changes, edema and hypertension are not obvious, plasma complement and C3 are reduced, and there are still manifestations of extra-renal symptoms, such as circulatory congestion, as the main clinical manifestations. Those who have no or slight changes in urine routine are easy to ignore. The following items can be used as a reference for diagnosis.
The main diagnosis basis: 1 history of pre-infection, such as acute tonsillitis, pyoderma, scarlet fever. 2 different degrees of edema. 3 extrarenal symptoms such as hypertension, heart or kidney dysfunction, hypertensive encephalopathy.
Secondary diagnosis is based on: 1 anti-streptolysin O (ASO) and increased erythrocyte sedimentation rate. 2 plasma total complement or C3 value decreased. 3 serum circulating immune complexes increased. If there are 1 to 2 major diagnostic criteria and 1 minor diagnosis, it can be diagnosed as extrarenal symptomatic nephritis. Renal biopsy is an important method for diagnosing this disease, and its pathological changes are consistent with typical acute post-chain nephritis.
(2) Nephrotic syndrome: severe edema may occur in the early stage of the disease or in the course of the disease, and the increase in urinary protein is usually more than 3.5g per day. Urinary FDP is often elevated with high blood pressure. It is difficult to distinguish only the clinical manifestations from the pathological types of other kidney diseases.
(3) Rapid progressive nephritis: acute streptococcal infection after acute nephritis due to a large number of crescent formation in the renal capsule, while endothelial cells, mesangial cells continue to proliferate, the clinical manifestations of acute nephritis, severe renal damage, rapid entry Acute renal failure. Therefore, when the acute chain-sensing nephritis is 2 to 4 weeks, the edema does not retreat, the amount of urine decreases, the blood pressure continues to increase, and even the heart and brain damage may occur. The possibility of acute nephritis should be considered. At this time, a renal biopsy is helpful for diagnosis and differential diagnosis.
Typical cases of hematuria, proteinuria, oliguria, edema, hypertension, etc. in a short period of time, severe pulmonary congestion or pulmonary edema, can be diagnosed as acute nephritic syndrome; pharyngeal infection or skin infection history 1 to 3 weeks before the disease With regard to streptococcus culture and serological test positive, serum complement decline, CIC rise, etc., can help diagnose the disease in the clinic. If the clinical manifestations are not obvious, multiple routine urine tests should be performed, and the diagnosis should be made according to the typical changes of urine and the dynamic changes of blood complement. There is only a history of streptococcal infection and the urine test is basically normal. Perform a renal biopsy if necessary.
Examine
Examination of nephritis after acute infection in the elderly
Urine routine
In addition to red blood cells and proteinuria, various types of tube (red blood cells, granules, white blood cells), and white blood cells, even with white blood cell casts, but not urinary tract infections, can be seen without urine changes, urine routine The change is slower than the clinical symptoms, especially the red blood cells often prolonged for several months to more than one year. The persistence of a large amount of proteinuria suggests the presence of nephrotic syndrome.
2. Blood routine
When edema is diluted by blood, hemoglobin and red blood cells can be reduced, diuretic edema can be restored, and white blood cell count is normal, but white blood cells and neutrophils can be increased with infection.
3. Renal function
There are many degrees of renal dysfunction, glomerular filtration rate and endogenous creatinine clearance are decreased, serum urea nitrogen and creatinine are temporarily increased during oliguria, and significant azotemia can occur with acute renal failure. Metabolic acidosis and other electrolyte disorders, renal blood flow decreased significantly in patients with heart failure.
4. Immunology and complement system examination
Anti-streptolysin O (ASO), anti-streptokinase (ASK), anti-hyaluronidase (AH), anti-deoxyribonuclease (ADNase) increased, indicating that most of this glomerulonephritis is chain-like Nephritis, ASO increased accounted for 70% to 80%, such as the simultaneous detection of the above three indicators positive rate of up to 100%, the early use of penicillin treatment ASO positive rate can be reduced to 15%, serum IgG, IgM increased, on the onset 1 2 months returned to normal; IgA was basically normal, 32% to 42% of patients had rheumatoid factor increased in the first week of onset, and serum cryoglobulin and circulating immune complexes were found in the first few weeks of onset.
Serum total complement (CH5O), C3 decreased in more than 90% onset within 2 weeks, and returned to normal after 4 to 6 weeks. If it continues to decrease, kidney disease is still going on, C2, C4 and preparation are also reduced, but reduced. The degree of C3 is clinically valuable for patients with mild type. The determination of serum complement is not only helpful for diagnosis, but also indicates the involvement of the complement system in the pathogenesis of acute chain-induced nephritis.
Combined with acute heart failure, X-ray showed chest enlargement and enlarged hilar shadows on both sides.
Diagnosis
Diagnosis and diagnosis of acute nephritis in elderly patients
Diagnostic criteria
1 history of pre-infection such as acute tonsillitis, pyoderma, scarlet fever and so on.
2 different degrees of edema.
3 extrarenal symptoms such as hypertension, heart or kidney dysfunction, hypertensive encephalopathy.
The secondary diagnosis basis is:
1 anti-streptolysin O (ASO) and increased erythrocyte sedimentation rate.
2 plasma total complement or C3 value decreased.
3 serum circulating immune complexes increased, such as primary diagnostic criteria 1 to 2 and secondary diagnosis can be diagnosed as extrarenal symptomatic nephritis, renal biopsy is an important method for the diagnosis of this disease, its pathological changes and typical acute chain Post-sensitization nephritis is consistent.
(2) Nephrotic syndrome: severe edema may occur in the early stage of the disease or in the course of the disease. The increase of urinary protein is usually above 3.5g per day, and the urinary FDP is often increased, accompanied by hypertension, only by clinical manifestations and pathology of other kidney diseases. Type identification is difficult.
(3) Rapid progressive nephritis: acute streptococcal infection after acute nephritis due to a large number of crescent formation in the renal capsule, while endothelial cells, mesangial cells continue to proliferate, the clinical manifestations of rapid progressive nephritis, severe renal damage, rapid entry Acute renal failure, therefore, when acute chain-sensing nephritis in the course of 2 to 4 weeks of disease, edema does not retreat, urine output decreases, blood pressure continues to increase, and even the involvement of the heart, brain damage, should consider the possibility of rapid progressive nephritis, at this time Kidney biopsy can help diagnose and differentiate diagnoses.
Short-term occurrence of hematuria, proteinuria, oliguria, edema, hypertension and other typical cases, severe pulmonary congestion or pulmonary edema, can be diagnosed as acute nephritis syndrome; pharyngeal infection or skin infection history 1 to 3 weeks before the disease For streptococcal culture and serological tests, serum complement decreased, CIC increased, etc., can help to confirm the disease in clinical, clinical manifestations are not obvious, multiple consecutive routine urine tests, according to typical changes in urine and blood complement dynamics Change the diagnosis, only the history of streptococcal infection and the urine test is basically normal, if necessary, do a renal biopsy.
Differential diagnosis
The following diseases should be excluded when diagnosing acute nephritis:
Acute systemic infection
Transient proteinuria and microscopic hematuria may occur during hyperthermia, which may be related to increased renal blood flow, increased glomerular permeability, and edema of renal tubular epithelial cells. This type of urinary change occurs in infections and high fever. With the fever, the urine test returned to normal, without the clinical manifestations of kidney disease such as edema and hypertension.
2. Acute urinary tract infection or acute pyelonephritis
Acute nephritis may have low back pain, oliguria and urinary red blood cells, there are also urination discomfort, urinary white blood cells can also be more, so it needs to be differentiated from urinary tract infection, but urinary tract infections have systemic and local infections Performance, such as fever, urinary tract irritation, a large number of white blood cells in the urine or even leukocyte casts, urinary bacterial culture positive, the efficacy of anti-infective treatment is also helpful to identify.
3. Rapid progressive nephritis
The onset process is very similar to the disease, but the patient is progressive oliguria, renal failure without urinary and rapid development, and eventually uremia. If acute nephritis syndrome is not relieved for more than 1 month, it is necessary to promptly perform renal thrombolysis. Identification of the disease.
4. Mesangial capillary nephritis
The onset process is very similar to this disease. It can also have a history of respiratory infection and even streptococcal infection. About 40% of patients have typical acute nephritic syndrome with hypocomplementemia, and even serum ASO titers can rise. Clinical process It is difficult to identify. According to a group of 20 patients with clinical diagnosis of this disease, 12 cases were confirmed by mesenteric capillary mesangitis, but mesangial capillary nephritis has no self-healing tendency, so the diagnosis is the disease. If the disease duration is more than 2 months, no reduction in mesangial capillary nephritis should be considered, and renal biopsy can help diagnose.
