Infective endocarditis renal damage (alias: infective endocarditis renal damage) What causes infective endocarditis renal damage? The causes of infective endocarditis are related to the following factors.
1. underlying disease
Patients with infective endocarditis often have underlying cardiovascular disease. Rheumatic heart disease accounts for 60% to 80% of the total incidence, with mitral valve (especially mitral valve prolapse) and aortic valve insufficiency being the most common, and tricuspid or pulmonary valve lesions being less common. Among congenital heart diseases, ventricular septal defect and ductus arteriosus is the most common, followed by bilobed aortic valve, tetralogy of Fallot and ruptured aortic sinus aneurysm. Other diseases such as Marfon syndrome, syphilitic heart disease and hypertrophic cardiomyopathy can also be caused.
The susceptibility to infective endocarditis may be due to blood flow from a high pressure cardiac cavity or vessel to a low pressure cardiac cavity or tubular cavity via a narrow cavity, creating a vortex due to the siphon pressure effect (venturi pressure effect), or due to jet damage (MacCallum spots), causing damage to the endocardium or heart valves, exposing collagen tissue leading to platelets and fibrinogen on the valves On the basis of this, microorganisms can easily implant on the aseptic redundancy, causing infective endocarditis.
Infective endocarditis can also be caused by medical factors, including interventional cardiovascular consultations and cardiac or noncardiac surgery, intracardiac pressure monitoring intubation, atrioventricular shunts, high-energy nutrition, biopsies, pacemakers, arteriovenous cannulation, catheters, and tracheal intubation (especially in burn patients with reduced resistance). 2% to 6% of patients on long-term hemodialysis develop infective endocarditis. Those with malignant tumors treated with chemotherapy, bone marrow or immunosuppressive therapy after organ transplantation, as well as patients with drug addiction and AIDS, are susceptible to this disease.
2. Pathogens
Acute infective endocarditis is mostly caused by the invasion of intensely virulent bacteria into the endocardium. Staphylococcus aureus infection is the main cause of acute infective endocarditis and is also the main causative agent in patients with drug addiction and prosthetic valves. These patients often have systemic bacterial dissemination, including skin, bone, joint, eye, and brain. 5% to 10% of patients with drug-addicted and prosthetic valve infective endocarditis are caused by gram-negative bacteria. Infective endocarditis caused by anaerobic bacterial infections accounts for about 1% of cases, probably due to the high oxygen content of intracardiac blood which is not conducive to the growth of anaerobic bacteria.
Subacute infective endocarditis is generally caused by less virulent bacteria, with Streptococcus straw green being the majority, followed by Enterococcus and Cryptococcus in that order. Previous reports indicate that 80% of non-prosthetic infective endocarditis is caused by streptococci or staphylococci. The pathogenic pathways of invasion are through the oral cavity, urinary tract, lung and intestinal foci of infection into the bloodstream. In normal subjects, these pathogens are readily destroyed by the body, but in the case of heart valve lesions, they tend to retain bacteria and cause infective endocarditis. The site of microbial invasion is often located in front of the narrow orifice through which blood flows, for example, on the atrial surface of the valve leaflets in mitral valve insufficiency; on the endocardium of the right ventricle in ventricular septal defect; and on the endocardium of the pulmonary artery in arteriovenous catheterization. Patients with drug addiction or AIDS often have tricuspid infective endocarditis with recurrent pulmonary infarction and fungal infective endocarditis of the mitral and aortic valves with limb artery embolism.
Abscess formation is one of the serious complications of valve infection and can result from direct invasion of the fibrous cardiac skeleton (i.e., perivalvular connective tissue) by the infectious focus, with involvement of adjacent myocardium. Occasionally, hematogenous dissemination leads to extracardiac abscess formation. Abscess formation is most often seen in acute infective endocarditis and is rare in subacute infective endocarditis.
3.Immunological factors
Bacteria in the endocardial flab stimulate the immune system to produce nonspecific antibodies, resulting in an increase in multiple strains of gamma globulin, a positive rheumatoid factor, and an occasional positive syphilis serologic test invasion. Positive rheumatoid factor is seen in half of patients with subacute infective endocarditis, provides a clue to the diagnosis of the disease in patients with negative blood cultures, and turns negative when the bacteria are killed. anti-endocardial and anti-myofibrillar antibodies are present in 60% to 100% of patients with infective endocarditis (especially subacute infective endocarditis).
Specific antibodies against a wide range of bacteria are already present in most patients prior to bacterial infection, the latter being further increased during exacerbation of the infection and reduced by treatment. Apparently, such specific antibodies have no role in the prevention of endocardial infection and reinfection.
Serum hemolysis complement is reduced in about 30% of patients with infective endocarditis, increases with treatment, and turns normal. Immune complex glomerulonephritis patients have reduced hemolysis complement, and circulating immune complexes are present in 82% to 97% of patients with infective endocarditis. When the latter concentration is increased, patients often have extracardiac manifestations such as arthritis, splenomegaly, glomerulonephritis, prolonged disease duration, and hypocomplementemia. Certain studies have confirmed that glomerulonephritis in patients with infective endocarditis is caused by the immune complex. Similarly, arthritis, synovitis, pericarditis, Osler’s nodes, and Roth’s hemorrhagic spots are also inflammatory reactions due to the immune complex.
Pathogenesis of infective endocardium causing renal damage is generally considered to be microembolism as the cause of focal nephritis, but immunofluorescence and electron microscopy provide important evidence for the pathogenesis of immune complexes. Immunofluorescence staining in diffuse and focal glomerulonephritis showed similar manifestations, mainly as diffuse granular C3 deposition along the capillary wall. Immunoglobulin (mainly IgG) deposits are also present in the capillary wall and thylakoid region. Some immunofluorescent deposits in focal nephritis may also be seen in glomeruli that appear to be normal. Deposits with increased electron density are usually not seen in focal glomerulonephritis, whereas they occur frequently in diffuse glomerulonephritis, mostly between the glomerular basement membrane and endothelial cells and within the thylakoid membrane. In some patients, deposits can also be found within the glomerular basement membrane and between the pedicles of the epithelial cells. In patients with endocarditis due to coagulase-positive staphylococci, the deposits are mainly located under the epithelial cells, similar to the presentation of glomerulonephritis after acute streptococcal infection.
The bacteria causing infective endocarditis or their products act as antigens and produce corresponding antibodies, both of which form a circulating immune complex. The site of deposition of the immune complex in the glomerulus is related to the type of bacteria and the period of infection, but depends mainly on the size and solubility of the antigen-antibody complex. The immune complexes formed when there is an excess of antigen are small and highly soluble and are easily deposited under the glomerular epithelium, mostly in the septic phase of bacterial endocarditis, especially in coagulase-positive staphylococcal endocarditis, which is often accompanied by diffuse proliferative glomerulonephritis. When there are slightly more antibodies than antigens, the immune complexes formed are moderately voluminous and poorly soluble; when there are significantly more antibodies than antigens, the resulting larger immune complexes are insoluble. These moderate and large volume immune complexes are often deposited under the glomerular endothelium, causing focal or diffuse glomerulonephritis, mostly seen in subacute bacterial endocarditis due to Streptococcus straw green. In addition, antigen-antibody complexes can be found in the blood circulation. The disease also has complement activation and utilization, and antibodies have been obtained from diseased kidney tissue, the latter with positive immune reactions caused by bacteria obtained in blood cultures from the same patients. What are the manifestations of renal damage in infective endocarditis and how is it diagnosed?
1, renal manifestations
(1) Immune nephritis
Immune nephritis occurs mostly a few weeks after the onset of endocarditis and is consistent with the mechanism by which the immune response occurs. It is manifested by varying degrees of microscopic or carnal hematuria, proteinuria, and erythrocyte tubularity. Mild to moderate acute nephritis syndrome with azotemia is more common, with elevated blood urea and creatinine and decreased creatinine clearance. Extensive crescent formation in the kidney has also been reported, with clinical manifestations of acute nephritis. Some patients may present with hypoproteinemia and nephrogenic edema, while nephrotic syndrome is rare. Extensive and severe renal damage is common and renal failure may occur.
(2) Embolic nephritis
During the course of infective endocarditis, emboli of varying sizes can occur in the kidney, leading to embolic nephritis. The clinical manifestations depend on the size of the emboli as well as the site and degree of embolism. In small cases, the patient may have no symptoms, only microscopic hematuria or proteinuria; in large cases, severe back pain may occur suddenly, similar to renal colic caused by kidney stones, often with carnal hematuria.
(3) tubulointerstitial nephritis
Infective endocarditis causes interstitial nephritis and infectious pathogenic bacteria through the blood circulation into the renal parenchyma causing interstitial nephritis and long-term use of a large number of antibiotics, the use of antibiotics, especially penicillins, can lead to allergic tubulointerstitial nephritis. Its clinical manifestations are similar to other drug-related tubulointerstitial nephritis.
(4) Renal abscess
Acute staphylococcal endocarditis with concomitant systemic sepsis can lead to multiple small abscesses in the kidney at the same time. Clinical manifestations are fever, lumbago, percussion pain in the kidney area, and hematuria may occur.
2.Extra-renal manifestations
There is often irregular fever of varying degrees, with body temperature of 37,5-39℃, flaccid type, higher in the afternoon and evening, accompanied by chills and night sweats. There are also non-specific symptoms such as general malaise, weakness, loss of appetite and weight loss. Patients often complain of headache, chest and back and muscle and joint pain. On physical examination, there is a variable cardiac murmur, which may be an enhancement of an existing pathologic murmur or the appearance of a new pathologic murmur. about 70% of patients present with embolism, which manifests as petechiae on the lid conjunctiva, oral mucosa and skin, lobar hemorrhage under the finger or toenail, retinal Roth spots, Osler nodules and Janeway damage. The corresponding clinical manifestations may occur in the presence of visceral embolism such as cerebral embolism, pulmonary, splenic, mesenteric and submesenteric artery embolism that occurs later in the course of the disease. Patients mostly have progressive anemia, splenomegaly, elevated blood leukocytes, increased hematocrit, and 75% to 90% positive blood cultures for bacteremia.
(1) Common clinical manifestations of acute infective endocarditis
There is often a history of acute septic infection, recent surgery, trauma, puerperal fever or instrumental examination. The onset of the disease is acute, mainly manifesting as signs of sepsis, such as chills, hyperthermia, hyperhidrosis, debility, skin mucosal hemorrhage, shock, vascular embolism and migrating abscesses, and most of the original infectious lesions can be found.
The heart can have murmurs mainly for a short period of time, and they are variable and rough in nature. As valve damage is generally more severe, signs of acute valve closure insufficiency can be produced, with the mitral and/or aortic valves being the most clinically susceptible, and in a few cases, the pulmonary and/or tricuspid valves can be involved and produce the corresponding signs of valve closure insufficiency. In addition, it often causes acute cardiac insufficiency. If the lesion mainly invades the mitral or aortic valve, it may present as acute left heart insufficiency with pulmonary edema; if the lesion involves the tricuspid and pulmonary valves, it may present as signs of right heart failure; if both the left and right valves are involved, it may present as signs of total heart failure. If the redundant organisms are dislodged, the bacterial emboli may cause multiple embolisms and metastatic abscesses, and cause corresponding clinical manifestations.
(2) Subacute infective endocarditis has a slow onset and the initial clinical manifestations are atypical, especially in elderly patients, but most patients gradually develop characteristic manifestations. The disease should be considered in any cardiac patient with fever of unknown origin for more than 1 week. The fever is usually irregular and low or moderate, but there are cases of high fever and chills, joint and back pain. There is orthohemoglobinemia, pestle and mortar finger and splenomegaly. The heart may change in intensity or develop new murmurs in addition to the existing cardiac murmur, and the murmur is variable. Heart failure may also occur, mainly due to valve perforation, tendon rupture, functional stenosis, aortic sinus rupture and myocarditis or myocardial infarction due to coronary embolism during the course of endocarditis. Patients also have migratory infections and aneurysm formation. Embolism can cause various clinical manifestations, such as splenic embolism causing severe pain in the left upper abdomen, renal embolism causing hematuria and renal colic, cerebral embolism causing hemiparesis, aphasia, coma and subarachnoid hemorrhage as well as skin mucosal hemorrhage or streak-like hemorrhage, Osler’s nodes on the fingertips, retinal hemorrhage, etc.
In addition to the manifestations of renal damage (e.g. hematuria, proteinuria or hyperalgesia), there is a diagnostic basis consistent with endocarditis. Clinically typical endocarditis is now rare. Endocarditis should be suspected in patients with heart valve disease, congenital cardiovascular malformations, or prosthetic valve replacement who present with fever of unknown origin that persists for more than 1 week. Infective endocarditis-related nephropathy should be highly suspected if accompanied by changes in urinary routine.
However, in cases with atypical clinical presentation and negative blood cultures, care should be taken to differentiate them from active rheumatic heart disease, systemic lupus erythematosus, primary cryoglobulinemia, and systemic necrotizing vasculitis. The first two have specific indicators in laboratory tests, such as increased anti-nuclear and anti-DNA antibodies in patients with lupus erythematosus; single peak IgM is often detected in patients with cryoglobulinemia, and blood levels of cryoglobulin are generally higher than 10 g/L, accompanied by high titers of rheumatoid factor. Complement testing is mostly normal in systemic necrotizing vasculitis. What tests should be done for renal damage in infective endocarditis?
1.Blood test
(1) Blood culture: It is the main basis for confirming the diagnosis of the disease, and it can also follow up whether the bacteraemia persists. Blood culture should be done before the application of antibiotics, 75% to 85% of patients have positive blood culture, which is also the most direct evidence for the diagnosis of the disease. Take 10-20 ml of venous blood, preferably during high fever and chills, and take blood cultures several times to increase the positive rate. At the same time, anaerobic cultures should be made and kept for observation for at least 2 weeks. 15% to 20% of infective endocarditis blood cultures are negative, especially after cryptococcal and candida infective endocarditis and prolonged infective endocarditis with antibiotics. If venous blood cultures are negative, arterial blood, bone marrow or bolus cultures may be used if necessary. Diagnosis may also be made based on disease progression and response to treatment.
(2) General laboratory tests
Red blood cells and hemoglobin are reduced, with the latter mostly in the range of 6% to 10%g%. Occasionally, hemolysis may be present. Blood leukocytes are elevated or normal, mononuclear cells may be present in the classification, increased sedimentation, increased serum gamma globulin, increased IgG and IgM, decreased complement, and positive rheumatoid factor.
In patients with acute infective endocarditis, a significant increase in blood leukocytes and a leftward shift of neutrophil nuclei, sometimes with toxic granules, are common in routine blood tests. In addition, progressive anemia may be present. Blood cultures are easily positive for pathogenic bacteria, most of which are septic.
(3) Serum immunological examination
In subacute infective endocarditis of up to 6 weeks duration, 50% of rheumatoid factors are positive, and their potency can decrease rapidly after antibiotic treatment. Sometimes hypergammaglobulinemia or hypocomplementemia may occur, commonly in patients with concomitant glomerulonephritis, and the level of decline is often consistent with poor renal function. Circulating immune complex CIC is positive in about 90% of patients and is often above 100?g/ml, which is higher than in septic patients without endocarditis and has differential diagnostic value, especially in those with negative blood cultures. Other tests include precipitating antibody assay, agglutinin reaction and complement binding test in fungal infections. Staphylococcus aureus is measured by antibodies to cytosolic acid, etc.
2.Urine analysis
More than half of the patients may have proteinuria and microscopic hematuria or carnivorous hematuria, polymorphic red blood cells, a few may have tubular red blood cells, mild proteinuria, but pusuria or tubular urine may also occur occasionally, and some urinary routine may also be normal. When renal failure occurs, there are corresponding changes, and blood urea nitrogen and creatinine are mildly increased, but severe or progressive renal failure can also occur.
The examination methods are as follows.
1.Renal biopsy pathological examination
In acute cases, only neutrophilic leukocyte and monocyte infiltration, endothelial and thylakoid cell proliferation are seen, whereas in patients with subacute endocarditis, the glomeruli show diffuse damage, with deposition of IgG, IgM and C3 in the subepithelial, subendothelial, intra-basement and thylakoid areas, proliferation of cells inside and outside the capillaries, and glomerulosclerosis is seen.
2.Electrocardiogram
It has no diagnostic value for uncomplicated infective endocarditis, but when incomplete or complete atrioventricular or bundle branch block or ventricular precontraction is present, it suggests high or low septal abscess or myocarditis. The prognosis is poor in those with ECG showing myocardial infarction or heart block. Newly developed heart block suggests abscess or aneurysm formation and often requires surgery.
3. Echocardiography
Echocardiography is valuable in the diagnosis of infective endocarditis and some of its intracardiac complications. The recent development of transesophageal 2D echocardiography is significantly superior to transthoracic wall 2D echocardiography. It is capable of detecting smaller bulges of 1 to 1.5 mm in diameter. It is not affected by the echoes caused by mechanical flaps and is more suitable for emphysema, obesity, and thoracic deformities. The diagnostic rate is greatly improved. It can also detect the extent of valve destruction or perforation, rupture of tendon cords, mitral or tricuspid valves with fetters, infected aortic aneurysms and mitral valve aneurysms due to endothelial damage to the anterior mitral leaflet ventricular surface caused by infected aortic regurgitation, and various septic intracardiac complications, hairy aortic root or annular abscesses, septal abscesses, myocardial abscesses, and septic pericarditis. It also helps to determine the original cardiac lesion, and the assessment of the severity of valvular regurgitation and left ventricular function can be used as a reference to judge the prognosis and determine whether surgery is needed.
4.Cardiac catheterization and cardiovascular angiography
Patients who respond well to antimicrobial therapy and do not have heart failure usually do not require this test. However, cardiac catheterization and cardiovascular angiography can provide important information when surgery is considered when medical therapy has failed, such as anatomic abnormalities including valve damage, congenital defects, coronary artery disease, aortic constriction, or fungal aneurysms. Cardiac output, right and left heart pressures, and the degree of mitral or aortic regurgitation can also be measured to determine when to perform valve replacement. Some people have taken blood specimens from the proximal and distal ends of the valve via cardiac catheterization to determine the difference in bacterial counts and believe that the site of infection can be determined. However, cardiac catheterization and cardiovascular imaging may cause embolism caused by dislodgement of the redundant organisms, or cause serious arrhythmias and aggravate heart failure, which should be considered carefully and the indications should be strictly controlled.
5.Radionuclide 67Ga(crop) heart scan
It is useful for the diagnosis of inflammation site of endocarditis and myocardial abscess, but it takes 72h 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 is not very valuable.
6.Imaging examination
(1)Chest X-ray examination is only helpful for the diagnosis of complications such as heart failure and pulmonary infarction. When patients with replacement prosthetic valves are found to have abnormal shaking or displacement of the valve, it suggests possible combined infective endocarditis.
(2) Computed tomography (CT) or spiral CT is useful in the diagnosis of large periaortic valve abscesses. However, the artifacts of the prosthetic valve and the pulsation of the heart affect its valuation of valve morphology, and its dependence on contrast and limited cross-sectional views limits its clinical application.
(3) Magnetic resonance imaging (MRI) is not affected by prosthetic valve artifacts and can be useful as an adjunct when aortic root abscesses cannot be excluded by 2-dimensional echocardiography; however, it is more expensive.
Complications such as heart failure, embolism, metastatic abscesses and infected aneurysms often occur.
1.Heart failure
Patients with acute infective endocarditis have mitral and aortic valves that are most susceptible to involvement, with severe valve damage producing acute valve closure insufficiency, which can manifest as acute left heart insufficiency and pulmonary edema. If the lesion involves the tricuspid valve and pulmonary valve, right heart failure may be seen. If both left and right heart valves are involved, signs of total heart failure may occur.
2.Embolism
If the redundant organisms are dislodged, the emboli with bacteria can cause multiple embolisms. The most common sites are brain, kidney, spleen and coronary artery, which can produce corresponding clinical manifestations.
3.Metastatic abscess
In acute infective endocarditis, the redundant organisms are easily dislodged, and these bacterial emboli can reach various parts of the body with the blood and cause the formation of abscesses.
4.Infectious aneurysm
Mostly due to severe infection, pathogenic microorganisms erode the elastic tissue of the arterial wall, resulting in local dilatation of the artery. Aneurysms that occur in smaller arteries have a better prognosis, while those that occur in larger arteries have a worse prognosis once they rupture.
5. Embolic nephritis
During the course of infective endocarditis, embolism of varying sizes can occur in the kidney and can be complicated by embolic nephritis. In particular, acute staphylococcal endocarditis with systemic sepsis can lead to multiple small abscesses in the kidney, and extensive and severe kidney damage can also cause acute nephritis and renal failure.