Infective endocarditis kidney damage

Introduction to Infective Endocarditis and Renal Damage Infective endocarditis (IE) is an inflammation of the heart valve or ventricular wall that is directly infected by microorganisms (bacteria, fungi and other microorganisms such as viruses, rickettsia, chlamydia, spirochetes, etc.), including acute And subacute endocardial inflammation. There are two types of renal damage caused by infective endocardium, one caused by micro or large emboli, called embolic nephritis or renal infarction. The other is caused by immune abnormalities called immunoneuritis, including focal glomerulonephritis, focal glomerular necrosis and diffuse glomerulonephritis, histological changes similar to streptococcal infection after nephritis. basic knowledge The proportion of the disease: the incidence of this disease in infective endometritis is about 0.02% -0.08% Susceptible people: no specific population Mode of transmission: pathogen transmission Complications: heart failure, abscess, aneurysm, sepsis, rapid progressive nephritis

Causes of infective endocarditis and renal damage

Cardiovascular disease (30%):

Patients with infective endocarditis often have underlying cardiovascular disease, and rheumatic heart disease accounts for 60% to 80% of the total number of cases, of which mitral valve (especially mitral valve prolapse) and aortic regurgitation are the most common. There are fewer tricuspid or pulmonary valve lesions. The most common type of ventricular septal defect and patent ductus arteriosus in congenital heart disease, followed by bicuspid aortic valve, tetralogy of Fallot and rupture of aortic sinus aneurysm, etc. Other diseases such as horse syndrome, syphilitic heart disease and hypertrophic cardiomyopathy can also be caused.

The cause of infective endocarditis may be due to blood flow from a high pressure heart chamber or blood vessel through a narrow empty channel to a low pressure heart chamber or lumen, resulting in a venturi pressure effect to form a vortex. Or due to jet damage (MacCallum plaque), causing damage to the endocardium or heart valve, causing collagen tissue exposure to cause platelets, fibrinogen to accumulate on the valve, on the basis of which microorganisms can be easily planted on aseptic sputum, Causes infective endocarditis.

Infective endocarditis can also be caused by iatrogenic factors, including cardiovascular interventional and cardiac or non-cardiac surgery, intracardiac pressure monitoring intubation, atrioventricular shunt, high-energy nutrition, biopsy, pacemaker, arteriovenous Intubation, catheter, tracheal intubation (especially in patients with burns, reduced resistance), 2% to 6% long-term hemodialysis patients with infective endocarditis, malignant tumors received chemotherapy, bone marrow or organ transplantation Immunosuppressive therapists, as well as drug users and AIDS patients, are susceptible to the disease.

Pathogen (20%):

Acute infective endocarditis is mostly caused by invasive endocardium by highly toxic bacteria. Staphylococcus aureus infection is the main cause of acute infective endocarditis and the main pathogen of patients with drug and artificial valves. These patients often have systemic bacterial dissemination, including skin, bone, joints, eyes and brain, 5% to 10% of patients with drug-induced and endocardial infective endocarditis caused by Gram-negative bacteria, anaerobic infection The infective endocarditis caused by about 1% may be due to the high oxygen content in the blood of the heart and is not conducive to the growth of anaerobic bacteria.

Subacute infective endocarditis is generally caused by bacteria with low virulence, and the majority of Streptococcus viridans are Enterococcus and Cryptococcus, etc. Previous reports indicate that infective endocarditis with non-prosthetic valves At the time, 80% is caused by streptococcus or staphylococcus. The path of pathogen invasion enters the blood through the oral cavity, urinary tract, lung and intestinal infection. In normal people, these pathogens can be eliminated by the body at any time, but in the heart valve. When the lesion is diseased, it is easy to retain bacteria, causing infective endocarditis. The part invaded by the microorganism is often located in front of the narrow blood channel, such as the atrial surface of the leaflet when the mitral regurgitation is closed. Intraventricular membrane; in the intima of the pulmonary artery during patent ductus arteriosus, patients with drug or AIDS often have tricuspid infective endocarditis with repeated pulmonary infarction, mitral and aortic valve fungal infective endocarditis Limb arterial embolism.

Abscess formation is one of the serious complications of valve infection, which can be caused by the direct invasion of the fibrous heart skeleton (ie, connective tissue around the valve), and involves adjacent myocardium. Occasionally, blood-borne dissemination leads to extracardiac abscess formation, abscess The formation is more common in acute infective endocarditis, and subacute infective endocarditis is rare.

Immunological factors (15%):

Bacteria in endocardial neoplasms stimulate the immune system to produce non-specific antibodies, resulting in increased gamma globulin, rheumatoid factor-positive, accidental syphilis serum test positive, rheumatoid factor positive in half of subacute infective endocarditis The patient provides clues for the diagnosis of this disease in patients with negative blood culture, and turns negative after the bacteria are killed. 60% to 100% of patients with infective endocarditis (especially subacute infective endocarditis) have antibiotics. Endocardial and anti-muscle membrane antibodies.

Prior to bacterial infection, most patients already have specific antibodies against a variety of bacteria, which are further increased when the infection is aggravated, and reduced after treatment. Obviously, this specific antibody prevents endocardial infection and reinfection. effect.

About 30% of patients with infective endocarditis have reduced serum hemolytic complement, which is increased after treatment and turned into normal. The hemolytic complement of patients with immune complex glomerulonephritis is reduced, and 82% to 97% of patients with infective endocarditis exist. Circulating immune complexes, when the latter concentration increases, patients often have extracardiac manifestations, such as arthritis, splenomegaly, glomerulonephritis, prolonged disease, hypo-complementemia, some studies have confirmed, infective endocarditis The patient's glomerulonephritis is caused by the immune complex. Similarly, arthritis, synovitis, pericarditis, Osler nodules, and Roth hemorrhage are also inflammatory responses caused by immune complexes.

Pathogenesis

The pathogenesis of infective endocardium-induced renal damage is generally considered to be the cause of focal nephritis, but immunofluorescence and electron microscopy provide important evidence for the pathogenesis of immune complexes, diffuse and focal kidney The immunofluorescence staining of glomerulonephritis is similar, mainly characterized by diffuse granular C3 deposition along the capillary wall, deposition of immunoglobulin (mainly IgG) in the capillary wall and mesangial area, and some focal effects. Immunofluorescent deposits in nephritis can also be seen in glomeruli that appear to be normal, usually with a deposit of increased electron density in focal glomerulonephritis, whereas in diffuse glomerulonephritis Often occurring, mostly located between the glomerular basement membrane and endothelial cells and within the mesentery, some patients may also have sediments in the glomerular basement membrane and between the epithelial cell foot processes, in coagulase-positive grapes In patients with endocarditis caused by cocci, the sediment is mainly located under epithelial cells, which is similar to glomerulonephritis after acute streptococcal infection.

The bacteria causing infective endocarditis or its products act as antigens, and produce corresponding antibodies, which form a circulating immune complex. The deposition site of the immune complex in the glomerulus is related to the type of bacteria and the infection period, but mainly depends on In the size and solubility of the antigen-antibody complex, the immune complex formed when the antigen is excessive, the volume is small and the solubility is high, and it is easy to deposit under the glomerular epithelial cells, which is more common in the sepsis phase of bacterial endocarditis. , especially coagulase-positive staphylococcal endocarditis, often accompanied by diffuse proliferative glomerulonephritis, when the antibody is slightly more than the antigen, the immune complex formed is moderately volumed and has poor solubility; When the antibody is significantly more than the antigen, the resulting large immune complex is insoluble. These moderate and large-volume immune complexes often deposit under the glomerular endothelium, causing focal or diffuse glomerulonephritis. It is more common in subacute bacterial endocarditis caused by Streptococcus viridans. In addition, antigen-antibody complexes can be found in the blood circulation. There is still complement activation and utilization in this disease. Antibody made from human kidney tissue lesions, the latter with the same patient blood culture for a positive immune response to bacteria.

Infective endocarditis, prevention of kidney damage

First of all, we must eliminate the incentives and treatment of the primary disease, and actively prevent and treat various infections such as oral infections, skin infections, urinary tract infections and pneumonia to reduce the incidence of infective endocarditis. Many scholars have found that it often occurs after tooth extraction. Temporary bacteremia, especially in cases with periodontal disease or simultaneous removal of many teeth, many oral bacteria can enter the blood through the wound, but most common with Streptococcus viridans, digestive tract and genitourinary system Trauma and infection often cause enterococci and Gram-negative bacilli. Staphylococcal bacteremia is seen in the skin and infections away from the heart. Therefore, it is appropriate to prevent prophylactic use from antibacterial bacteremia, but it is necessary to prevent this disease with antibiotics. Be active and avoid abuse.

In addition, we must adhere to prevention, publicize the dangers of this disease and advise people to stay away from drugs, and rely on intravenous drug dependence to persuade them to actively detoxify to reduce the incidence of cardiac infective endocarditis and effectively prevent infection. Endocarditis is also the main measure to prevent kidney damage.

Complications of infective endocarditis and renal damage Complications heart failure abscess aneurysm sepsis rapid progressive nephritis

Complications such as heart failure, embolism, metastatic abscess and infectious aneurysm often occur.

1. Heart failure: The mitral and aortic valves of patients with acute infective endocarditis are most susceptible, and the valve damage is severe, resulting in acute valvular insufficiency, acute left ventricular dysfunction, pulmonary edema, lesions Involvement of the tricuspid valve and pulmonary valve, the appearance of right heart failure can occur, if left and right heart valves are involved, it can produce signs of heart failure.

2. Embolism: If the sputum is shed, the emboli can cause multiple embolisms. The most common sites are the brain, kidney, spleen and coronary artery, which can produce corresponding clinical manifestations.

3. Metastatic abscess: The sputum of acute infective endocarditis is easy to fall off. These infected emboli can form the abscess with the blood reaching various parts of the body.

4. Infectious aneurysms: Due to serious infections, pathogenic microorganisms erode the elastic tissue of the arterial wall, leading to local expansion of the arteries, aneurysms occurring in smaller arteries, and a good prognosis. Once an aneurysm occurs in a larger artery, the prognosis Poor.

5. Embolization nephritis: In the course of infective endocarditis, the kidney may have embolism of varying sizes, which may be complicated by embolic nephritis, especially acute staphylococcal endocarditis accompanied by systemic sepsis. Causes multiple small abscesses in the kidneys. Extensive and severe renal damage can also cause acute nephritis and renal failure.

Infective endocarditis, symptoms of kidney damage, common symptoms, aseptic sputum, loss of appetite, high fever, hyperthermia, chills, leukocytosis, fever, hypoproteinemia, weakened retinal Roth plaque

1. Kidney performance

(1) Immune nephritis: Immune nephritis occurs more than a few weeks after the onset of endocarditis, in line with the mechanism of immune response, manifested as different degrees of microscopic or gross hematuria, proteinuria, red blood cell cast, light to medium Acute nephritis syndrome with azotemia is common, blood urea and creatinine are elevated, creatinine clearance is decreased, and there are reports of extensive crescent formation in the kidney, clinically rapid nephritis, and some patients may have hypoproteinemia. And renal edema, and nephrotic syndrome is rare, common extensive and severe kidney damage, renal failure can occur.

(2) embolic nephritis: in the course of infective endocarditis, the kidney may undergo embolism of varying sizes, leading to embolic nephritis, clinical manifestations depending on the size of the embolism and the embolization site, the degree may be Any symptoms are only microscopic hematuria or proteinuria; large ones can suddenly have severe low back pain, similar to renal colic caused by kidney stones, often with gross hematuria.

(3) tubulointerstitial nephritis: infective endocarditis causes interstitial nephritis and infection pathogens through the blood circulation into the renal parenchyma caused by interstitial nephritis and long-term use of a large number of antibiotics, the use of antibiotics, especially penicillins, can lead to allergic tubules Interstitial nephritis, its clinical manifestations are similar to other drug-related tubulointerstitial nephritis.

(4) renal abscess: acute staphylococcal endocarditis accompanied by systemic sepsis can also cause multiple small abscesses in the kidney, clinical manifestations of fever, low back pain, kidney area sputum pain, hematuria may occur.

2. Extrarenal performance

There are often irregular fevers of different degrees, body temperature 37.5 ~ 39 ° C, relaxation type, higher in the afternoon and evening, with chills and night sweats, as well as non-specific symptoms such as general malaise, weakness, loss of appetite and weight loss, patients Common complaints of headache, chest and back and muscle and joint pain, physical examination of variable heart murmur, may be the original pathological murmur enhanced or new pathological murmur, about 70% of patients with embolism, manifested as palpebral conjunctiva, oral Mucosal and skin imperfections, finger or nail rupture flakes, retinal Roth plaques, Osler nodules and Janeway lesions, visceral embolisms that occur later in the course of the disease such as cerebral embolism, lung, spleen, mesenteric and inferior mesenteric artery embolism may occur Corresponding clinical manifestations, patients with progressive anemia, splenomegaly, elevated white blood cells, increased erythrocyte sedimentation rate, blood culture 75% ~ 90% positive bacteremia.

(1) Common clinical manifestations of acute infective endocarditis: often with acute suppurative infection, recent surgery, trauma, history of calving fever or device examination, rapid onset, mainly manifested as signs of sepsis, such as chills, high fever , sweating, weakness, skin mucosal hemorrhage, shock, vascular embolism and migratory abscess, and more can find the original infection.

The heart is mainly murmur in the short term, and its nature is variable and rough. Because the valve damage is generally serious, it can produce signs of acute valvular insufficiency. Clinically, the mitral valve and/or aortic valve are the most susceptible. Cases may involve the pulmonary valve and/or the tricuspid valve, and produce signs of valvular insufficiency. In addition, acute cardiac dysfunction is often caused. If the lesion mainly invades the mitral or aortic valve, it is characterized by acute left ventricular function. Incomplete, pulmonary edema; if the lesion involves the tricuspid valve and pulmonary valve, it can be a sign of right heart failure; if left and right heart valves are involved, it can produce signs of heart failure, if the sputum is shed, the bacteria Embolism can cause multiple embolisms and metastatic abscesses, and cause corresponding clinical manifestations.

(2) Subacute infective endocarditis has a slow onset, and the initial clinical manifestations may be atypical, especially in elderly patients, but most patients gradually show characteristic manifestations. All patients with heart disease have unexplained fever for more than 1 week. Considering the possibility of this disease, fever is often irregular low fever or moderate fever, but there are also high fever chills, joints and low back pain, positive hemoglobin anemia, clubbing and splenomegaly, the heart in addition to the original heart disease murmur, its intensity Changes may occur or new murmurs may occur, and noise may be variable, and heart failure may occur, mainly during endocarditis, valve perforation, chordae rupture, functional stenosis, aortic sinus rupture, and coronary artery embolism Caused by myocarditis or myocardial infarction, patients with migration infections and aneurysm formation, embolism can cause various clinical manifestations, such as splenic embolism can cause severe pain in the left upper abdomen, renal embolism can cause hematuria and renal colic, cerebral embolism Can cause hemiplegia, aphasia, coma and subarachnoid hemorrhage and skin mucosal hemorrhage or streaking hemorrhage, Osler nodules at the fingertips, retinal hemorrhage, etc.

In addition to the manifestations of renal damage (such as hematuria, proteinuria or renal dysfunction, etc.), there is still a diagnosis basis for endocarditis. At present, typical clinical endocarditis is rare, for heart valve disease, Patients with congenital cardiovascular malformation or artificial valve replacement, who have unexplained fever for more than 1 week, should be suspected of endocarditis. If accompanied by changes in urine routine, it should be highly suspected of infective endocarditis. Kidney disease.

However, for patients with atypical clinical manifestations and negative blood culture, attention should be paid to the identification of rheumatoid heart disease, systemic lupus erythematosus, primary cryoglobulinemia and systemic necrotizing vasculitis. There are specific indicators in the middle, such as anti-nuclear antibodies and anti-DNA antibodies in patients with lupus erythematosus; patients with cryoglobulinemia can often detect peak IgM, blood cholesterol levels are generally higher than 10g / L With high titer rheumatoid factor, systemic necrotizing vasculitis complement detection is mostly normal.

Inflammatory endocarditis renal damage examination

Blood test

(1) Blood culture: It is the main basis for the diagnosis of this disease, and it is also possible to follow up whether bacteremia persists. Blood culture should be done before antibiotic application. 75%-85% of patients have positive blood culture, which is also a diagnosis of this disease. The most direct evidence, taking venous blood 10 ~ 20ml, it is best to collect blood in high heat chills, and blood collection culture to increase the positive rate, and should be used for anaerobic culture, at least for 2 weeks, 15% to 20% infection Endocardial blood culture is negative, especially cryptococcal, candida infective endocarditis and long-term infective endocarditis after the application of antibiotics, if the venous blood culture is negative, if necessary, arterial blood, bone marrow Or embolization, can also be diagnosed according to the development of the disease and treatment response.

(2) General laboratory tests: red blood cells and hemoglobin are reduced, the latter are mostly in 6% to 10g%, occasionally there may be hemolysis, white blood cells increase or normal, there may be mononuclear cells in the classification, ESR increased, serum gamma balls Protein increased, IgG, IgM increased, complement decreased, rheumatoid factor positive.

In patients with acute infective endocarditis, blood leukocytes are obviously increased, neutrophils are left-shifted, and there may be poisonous particles, sometimes left shifting. In addition, progressive anemia may occur, and blood culture is easily positive. Bacteria, and mostly purulent bacteria.

(3) Serum immunological examination for subacute infective endocarditis for up to 6 weeks, 50% of rheumatoid factor is positive, after antibiotic treatment, its titer can be rapidly decreased, sometimes high gamma globulin blood can occur Symptoms or hypocomplementemia, common in patients with complicated glomerulonephritis, the level of decline is often consistent with renal dysfunction, about 90% of patients with circulating immune complex CIC positive, and often above 100g / ml, than Patients with no endocarditis have high sepsis and have the value of differential diagnosis. Especially for those with negative blood culture, it is necessary to pay attention to systemic lupus erythematosus. The serum level of CIC in patients with hepatitis B surface antigen positive and other immune diseases can also be greater than 100g. /ml, other tests for the detection of precipitated antibodies in the presence of fungal infections, lectin response and complement binding assays, determination of muramic acid antibodies to S. aureus.

2. Urine analysis

More than half of patients may have proteinuria and microscopic hematuria or gross hematuria. Red blood cells are polymorphic, and a small number may have red blood cell casts and mild proteinuria, but pyuria or tubular urine occasionally occur, and some urine routines also occur. Normal, when renal failure occurs, the corresponding changes, blood urea nitrogen and creatinine increased slightly, but severe or progressive renal failure can also occur.

1. Renal biopsy pathological examination only seen neutrophil white blood cells, mononuclear cell infiltration, endothelial and mesangial cell proliferation, while subacute endocarditis patients with diffuse damage to the glomerulus, subepithelial, subendothelial, The deposition of IgG, IgM and C3 was observed in both the basement membrane and the mesangial area, and the cells inside and outside the capillaries proliferated, and glomerular sclerosis was observed.

2. Electrocardiogram has no diagnostic value for uncomplicated infective endocarditis, but when there is incomplete or complete atrioventricular or bundle branch block or ventricular premature contraction, it suggests high or low ventricular septal abscess or Myocarditis, ECG shows poor prognosis in patients with myocardial infarction or cardiac arrest, and the recent appearance of cardiac blockage suggests abscess or aneurysm formation, often requiring surgery.

3. Echocardiography is of great value in the diagnosis of infective endocarditis and some of its intracardiac complications. The recently developed transesophageal two-dimensional echocardiography is significantly superior to transthoracic wall two-dimensional echocardiography. The smaller neoplasm with a diameter of 1 to 1.5 mm is not affected by the echo caused by the mechanical valve, and is more suitable for emphysema, obesity, and thoracic deformity, which greatly improves the diagnosis rate and can detect the degree of valve destruction. Or perforation, chordae rupture, mitral or tricuspid valve, infective aortic aneurysm, and mitral valve caused by anterior mitral ventricular effusion damage caused by infected aortic regurgitation Tumor, as well as various suppurative intracardiac complications, aortic root or annulus abscess, ventricular septal abscess, myocardial abscess, suppurative pericarditis, etc., and help to determine the original heart disease, serious valvular regurgitation Assessment of degree and left ventricular function can be used as a reference for judging prognosis and determining whether surgery is needed.

4. Cardiac catheterization and cardiovascular angiography respond well to antibacterial therapy and patients without heart failure usually do not need this test, but when the medical treatment is not effective and the surgery is considered, cardiac catheterization and cardiovascular angiography can provide important information, such as Anatomical abnormalities include valvular lesions, congenital defects, coronary lesions, aortic coarctation, or fungal aneurysms. The same can be used to determine cardiac output, left and right heart pressure, and mitral or aortic regurgitation. At the time of valve replacement, some people took blood samples through the cardiac catheter at the proximal and distal ends of the valve to determine the difference in bacterial count. It is believed that the site of infection can be determined, but cardiac catheterization and cardiovascular imaging may cause the neoplasm to fall off. Cause embolism, or cause severe arrhythmia, aggravate heart failure, must be carefully considered, strict control of indications.

5. Radionuclide 67Ga (cow) heart scan is helpful for the diagnosis of inflammation and myocardial abscess in endocarditis, but it takes 72 hours to show positive, and the sensitivity and specificity are significantly worse than two-dimensional echocardiography. And there are more false negatives, so the clinical application value is not great.

6. Imaging examination

(1) Chest X-ray examination is only helpful for the diagnosis of complications such as heart failure and pulmonary infarction. When the patient with replacement artificial valve finds abnormal shaking or displacement of the valve, it may indicate that infective endocarditis may be associated.

(2) Computerized tomographic imaging (CT) or spiral CT has a certain diagnostic effect on suspected large aortic valve abscess, but the artifact of the artificial valve and the heart beat affect the shape of the valve. Valuation, and relying on contrast agents and limited cross-sections, limits their clinical application.

(3) Magnetic resonance imaging (MRI) Because of the influence of artificial valve artifacts, when the two-dimensional echocardiography can not exclude the aortic root abscess, it can play an auxiliary role, but the cost is more expensive.

Diagnosis and diagnosis of infective endocarditis with renal damage

Due to the diverse clinical manifestations of this disease, it is often confused with other diseases, with fever as the main manifestation and mild cardiac signs must be identified with typhoid fever, tuberculosis, upper respiratory tract infection, tumor, collagen tissue disease, etc., based on rheumatic heart disease. Occurrence of this disease, after a sufficient amount of antibiotic treatment and heat, heart failure does not improve, should be suspected of the possibility of combined rheumatism, this time should pay attention to check the changes in the pericardium and myocardium, such as the progressive enlargement of the heart with gallop, pericardium Friction sound or pericardial effusion, etc., but these two diseases can also exist at the same time, fever, heart murmur, embolization performance sometimes must be differentiated from atrial myxoma, the disease is mainly manifested by neurological or psychiatric symptoms, in the elderly should Attention should be paid to the differentiation of cerebral thrombosis, cerebral hemorrhage and mental changes caused by cerebral arteriosclerosis. The disease must be differentiated from the sepsis caused by Staphylococcus aureus Gram-negative bacilli. When embolism is prominent, it should be With cerebrovascular accidents, vasculitis, coronary heart disease, angina pectoris, acute glomerulonephritis, renal abscess, and embolic disease .

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