Infectious endocarditis and kidney damage

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

[1], [2], [3], [4]

Epidemiology

Among the systemic manifestations of infective endocarditis, an important place is occupied by diseases such as glomerulonephritis and vasculitis caused by immunocomplex lesions of capillaries of glomeruli and small vessels.

The prevalence of infectious endocarditis is 1.4-6.2 cases per 100 000 population. The increase in the incidence of infective endocarditis, noted in recent years, is associated with a wide spread of surgical interventions on the heart and the use of invasive instrumentation (intravascular catheters, arteriovenous fistulas and shunts, including for hemodialysis sessions), as well as the widespread spread of drug addiction. A special form of infective endocarditis - infectious endocarditis of drug addicts, associated with non-compliance with sterile conditions with intravenous injection of narcotic substances - occurs with a frequency of 1.5-2 cases per 1000 injecting drug users per year.

Men are 1.5-3 times more likely than women, and in the age group over 60 years - 5 times more often. In recent years, there has been a clear trend towards an increase in the incidence of elderly and senile patients, whose share in patients with infectious endocarditis in Russia today is 20%.

[5], [6], [7], [8], [9],

Causes of the kidney damage in infectious endocarditis

Infective endocarditis can cause various microorganisms, including fungi, rickettsia and chlamydia. However, bacteria are the causative agent first. The most frequent pathogens of infectious endocarditis are streptococci (50%) and staphylococci (35%). Other pathogens may be the bacteria of the group NASEC (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella), enterococci, pseudomonas, gram-negative bacteria of the intestinal group, etc. In a small part of the patients (5-15%), it is not possible to isolate the pathogen in repeated bacteriological studies of the blood. The reason for this in most cases is the previous antibiotic therapy. Features of the pathogen can affect the nature of the flow and the clinical features of infective endocarditis. Subacute infective endocarditis of damaged valves is most often caused by bacteria with low virulence (green streptococcus).

[10], [11], [12]

Symptoms of the kidney damage in infectious 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.
  • Nonspecific signs of infection and intoxication: fever, chills, night sweats, weakness, anorexia, weight loss,  arthralgia, myalgia, splenomegaly.
  • Specific signs of damage to the valves: the appearance or change in the nature of the noise as a result of the formation of valvular defects, the perforation of the valves, tearing of the tendon chords, rupture of the valve. These processes in more than 50% of patients are complicated by the development of circulatory insufficiency.
  • Arterial embolisms of fragments of vegetation: thromboembolism of cerebral vessels (acute disturbance of cerebral circulation), myocardial infarction, PE, occlusion of mesenteric arteries with the development of the "acute abdomen" pattern, spleen  infarction, kidney infarction, occlusion of large peripheral arteries (gangrene of the extremity).
  • Bacteremia with metastatic foci in organs: with high virulence of the pathogen, abscesses of the kidneys, myocardium, brain, etc. Develop.

[13], [14], [15]

Diagnostics of the kidney damage in infectious 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 the complement of CH50, and also the C3 and C4 components of the complement are often detected. Hypokomplementemia in infectious 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 complement C3-component in renal biopsy specimens during immunohistochemical examination. In addition, the content of complement in the blood in these patients can be considered as a marker of the effectiveness of antibiotic therapy. It was found that the slowed rate of normalization of the complement level is characteristic for persistent infection and indicates the need for correction of treatment.

[16], [17], [18], [19]

Treatment of the kidney damage in infectious endocarditis

Therapeutic tactics depends on the features of the pathogen, the localization and severity of valvular lesions, the presence of systemic manifestations of the disease (with the development of glomerulonephritis - from the state of kidney function). Antibacterial therapy is a method of etiotropic treatment of infective endocarditis. The basic principles of the use of antibacterial drugs are given below.

• It is necessary to use antibacterial drugs of bactericidal action.
• To create a high concentration of antibacterial drug in vegetation (which is necessary for effective treatment), intravenous administration of drugs in high doses for a long time (at least 4-6 weeks) is indicated.
• If the patient is in a serious condition and there is no evidence of an infectious agent, empirical therapy should be started before the results of a microbiological blood test.
• In the subacute flow of infective endocarditis or an uncharacteristic clinical picture, etiotropic antibacterial therapy should be performed after identifying the causative agent.