Infective endocarditis and kidney damage

Infective endocarditis is an inflammatory lesion of the heart valves and parietal endocardium of infectious etiology, which most often occurs as sepsis (acute or subacute) and is accompanied by bacteremia, valve destruction, embolic and immune (systemic) manifestations and complications.

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Epidemiology

Among the systemic manifestations of infective endocarditis, an important place is occupied by such diseases as glomerulonephritis and vasculitis, caused by immune complex damage to the glomerular capillaries and small vessels.

The prevalence of infective endocarditis is 1.4-6.2 cases per 100,000 population. The increase in the incidence of infective endocarditis observed in recent years is associated with the widespread use of cardiac surgeries and invasive instrumentation (intravascular catheters, arteriovenous fistulas and shunts, including for hemodialysis sessions), as well as with the widespread use of drug addiction. A special form of infective endocarditis - infective endocarditis of drug addicts, associated with failure to maintain sterile conditions during intravenous drug administration - occurs with a frequency of 1.5-2 cases per 1000 injection drug addicts per year.

Men get sick 1.5-3 times more often than women, and in the age group over 60 years - 5 times more often. In recent years, a clear trend towards an increase in the incidence of elderly and old people has been noted, the share of which among patients with infective endocarditis in Russia today is 20%.

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Causes kidney damage from infective endocarditis

Infective endocarditis can be caused by various microorganisms, including fungi, rickettsia and chlamydia. However, bacteria are the primary causative agent. The most common causative agents of infective endocarditis are streptococci (50%) and staphylococci (35%). Other causative agents may be bacteria of the HASEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella), enterococci, pseudomonads, gram-negative bacteria of the intestinal group, etc. In a small proportion of patients (5-15%), it is not possible to isolate the causative agent during repeated bacteriological blood tests. In most cases, this is due to previous antibacterial therapy. The characteristics of the causative agent may affect the nature of the course and clinical features of infective endocarditis. Subacute infective endocarditis of damaged valves is most often caused by bacteria with low virulence (viridans streptococcus).

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Symptoms kidney damage from infective endocarditis

Symptoms of infective endocarditis are caused by a combination of symptoms of infectious damage to the heart valves, thromboembolism from vegetation, bacteremia with metastatic foci in various organs and immunopathological processes.

• Infection on the valves.
  • Non-specific signs of infection and intoxication: fever, chills, night sweats, weakness, anorexia, weight loss, arthralgia, myalgia, splenomegaly.
  • Specific signs of valve damage: the appearance or change in the nature of noises as a result of the formation of valve defects, perforation of the valves, tearing of the tendinous chords, rupture of the valve. These processes are complicated by the development of circulatory failure in more than 50% of patients.
  • Arterial embolisms of vegetation fragments: thromboembolism of cerebral vessels (acute cerebrovascular accident), myocardial infarction, pulmonary embolism, occlusion of mesenteric arteries with the development of an “acute abdomen” picture, splenic infarction, renal infarction, occlusion of large peripheral arteries (gangrene of the limb).
  • Bacteremia with metastatic foci in organs: with high virulence of the pathogen, abscesses of the kidneys, myocardium, brain, etc. develop.

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Diagnostics kidney damage from infective endocarditis

Almost all patients with infective endocarditis have anemia and a significant increase in ESR, sometimes up to 70-80 mm/h. Neutrophilic leukocytosis or leukopenia, thrombocytopenia, an increase in the content of y-globulins, a high concentration of C-reactive protein, rheumatoid factor, circulating immune complexes, cryoglobulinemia, a decrease in the total hemolytic activity of complement CH50, as well as C3 and C4 components of complement are often detected. Hypocomplementemia in infective endocarditis serves as an indicator of kidney damage: in patients with glomerulonephritis, the frequency of its detection (94%) corresponds to the frequency of detection of deposits of the C3 component of complement in kidney biopsies during immunohistochemical examination. In addition, the content of complement in the blood of these patients can be considered as a marker of the effectiveness of antibacterial therapy. It has been established that a slow rate of normalization of complement levels is characteristic of persistent infection and indicates the need for treatment correction.

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Treatment kidney damage from infective endocarditis

Treatment tactics depend on the characteristics of the pathogen, localization and severity of the valve lesion, the presence of systemic manifestations of the disease (in the development of glomerulonephritis - on the state of kidney function). Antibacterial therapy is a method of etiotropic treatment of infective endocarditis. The main principles of using antibacterial drugs are given below.

• It is necessary to use antibacterial drugs with bactericidal action.
• To create a high concentration of the antibacterial drug in vegetations (which is necessary for effective treatment), intravenous administration of drugs in high doses over a long period of time (at least 4-6 weeks) is indicated.
• If the patient's condition is severe and there is no information about the infectious agent, empirical therapy should be started until the results of microbiological blood tests are available.
• In case of subacute infective endocarditis or atypical clinical picture, etiotropic antibacterial therapy should be carried out after identification of the pathogen.