Infective endocarditis and kidney damage: diagnosis

Laboratory diagnosis of 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.

An important diagnostic sign of infective endocarditis is bacteremia. The results of bacteriological examination of blood are positive in 70-85% of patients.

Instrumental diagnosis of kidney damage in infectious endocarditis

The main significance for the diagnosis of kidney damage in infectious endocarditis is Echocardiography, in which vegetation on the heart valves is detected. In case of doubtful results of transthoracic echocardiogram (sensitivity of the method in terms of vegetation diagnosis is 65%), transesophageal echocardiography (sensitivity is 85-90%) should be performed.

Differential diagnosis of kidney damage in infectious endocarditis

In typical cases, the diagnosis of kidney damage with infective endocarditis does not cause difficulties. Detection of vegetation on valves with transthoracic or transesophageal echocardiograms and a positive result of bacteriological examination of blood allows you to clearly verify the diagnosis, establish the etiology of the disease and prescribe adequate antibacterial therapy.

• Occurrence of urinary or acute syndrome in a patient with confirmed infective endocarditis before treatment with antibacterial drugs testifies, first of all, to the development of infectious glomerulonephritis, less often - about other variants of kidney damage peculiar to infective endocarditis.
• In the presence of urinary syndrome and impaired renal function that appeared against the background of antibacterial therapy, differential diagnosis of glomerulonephritis with drug nephropathy should be carried out. A kidney biopsy for most patients with infective endocarditis is not indicated.
• Subacute infective endocarditis, taking place with systemic manifestations (damage to the kidneys, skin, joints), must be differentiated from systemic lupus erythematosus, systemic vasculitis, malignant lymphoma. In differential diagnosis with systemic lupus erythematosus, the LE-cell phenomenon and the detection of antibodies to double-stranded DNA are crucial.
• Special difficulties are caused by differential diagnosis of subacute infective endocarditis with non-infectious thrombotic endocarditis in the primary or secondary (within the systemic lupus erythematosus) antiphospholipid syndrome. Antiphospholipid syndrome is diagnosed on the basis of the development of arterial and venous thrombosis, thrombocytopenia, a kind of skin lesion (reticulum). For thromboendocarditis in patients with antiphospholipid syndrome, in contrast to subacute infective endocarditis, mitral valve involvement is characteristic. Defining the diagnosis of antiphospholipid syndrome is the detection of antibodies to cardiolipin and / or lupus anticoagulant.

[1], [2], [3], [4], [5], [6]