Infective endocarditis and renal damage - Diagnosis

Laboratory diagnostics of kidney damage in 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 biopsy specimens 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.

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

Instrumental diagnostics of kidney damage in infective endocarditis

EchoCG is of primary importance for diagnosing kidney damage in infective endocarditis, as it reveals vegetations on the heart valves. In case of questionable results of transthoracic echoCG (the sensitivity of the method in terms of diagnosing vegetations is 65%), it is necessary to perform transesophageal echoCG (sensitivity is 85-90%).

Differential diagnosis of kidney damage in infective endocarditis

In typical cases, the diagnosis of kidney damage in infective endocarditis is not difficult. The detection of vegetation on the valves during transthoracic or transesophageal echocardiography and a positive result of bacteriological blood testing allow us to clearly verify the diagnosis, establish the etiology of the disease and prescribe adequate antibacterial therapy.

• The appearance of urinary or acute nephritic syndromes in a patient with confirmed infective endocarditis before the start of treatment with antibacterial drugs indicates, first of all, the development of infective glomerulonephritis, and less often, other types of kidney damage characteristic of infective endocarditis.
• In the presence of urinary syndrome and renal dysfunction that appeared against the background of antibacterial therapy, differential diagnostics of glomerulonephritis with drug-induced nephropathy should be performed. Kidney biopsy is not indicated for most patients with infective endocarditis.
• Subacute infective endocarditis with systemic manifestations (kidney, skin, joint damage) must be differentiated from systemic lupus erythematosus, systemic vasculitis, malignant lymphoma. In differential diagnostics with systemic lupus erythematosus, the LE-cell phenomenon and detection of antibodies to double-stranded DNA are of decisive importance.
• Particularly difficult is the differential diagnosis of subacute infective endocarditis with non-infective thrombotic endocarditis in primary or secondary (within systemic lupus erythematosus) antiphospholipid syndrome. Antiphospholipid syndrome is diagnosed based on the development of arterial and venous thromboses, thrombocytopenia, and a specific skin lesion (livedo reticularis). Unlike subacute infective endocarditis, thromboendocarditis in patients with antiphospholipid syndrome is characterized by mitral valve damage. The detection of antibodies to cardiolipin and/or lupus anticoagulant is decisive in the diagnosis of antiphospholipid syndrome.

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