Overview
Due to a variety of pathogens (mainly bacteria, but also viruses, mycoplasma, protozoa, etc.) enter the bloodstream, return to the heart cavity with the blood, grow and multiply in the heart lining, causing the endocardium to undergo damage of infective endocarditis and release toxins, which cause the body to become feverish and cause kidney damage. There are three main types of kidney damage caused by it: (1) immune nephritis; (2) embolic nephritis (renal infarction); and (3) focal nephritis caused by small infarct foci. Most of the disease can be cured if early diagnosis and timely use of appropriate antibiotics are made, but delayed diagnosis and treatment can lead to life-threatening or renal failure due to cardiac failure.
Etiology
Most cases of previous infective endocarditis occur in patients with pre-existing heart valve disease (e.g., rheumatic heart valve disease), congenital cardiovascular anomalies, and prosthetic valves. The incidence of infective endocarditis has declined with the use of antibiotics. However, the incidence of infective endocarditis has increased in recent years with the widespread use of cardiac surgery, endovascular interventions, intravenous nutrition, and hemodialysis intubation, as well as an increase in drug use. It is clear that the annual incidence of infective endocarditis in the intravenous drug use population in developed countries even exceeds that of patients with underlying heart disease. After prosthetic valve surgery, poor dental hygiene, chronic hemodialysis, and diabetes all increase the incidence of infective endocarditis. In developing countries, rheumatic fever remains the main causative agent of infective endocarditis.
The mechanism by which infective endocarditis leads to renal damage is poorly understood, and is now thought to be related to the formation of circulating immune complexes, which may manifest as focal or global glomerulonephritis, and in some patients, membranoproliferative glomerulonephritis or antiglomerular basement membrane antibody-type nephritis may occur; acute interstitial nephritis, a rare complication in such patients, is likely to be related to localized renal infections and the use of allergy-inducing medications.
Symptoms
1. Irregular fever.
2. Hepatosplenomegaly.
3. Osler nodules, Roth spots.
4. Pestle-like fingers.
5. glomerular damage (asymptomatic hematuria and/or proteinuria, acute nephritis syndrome, acute progressive nephritis syndrome, nephrotic syndrome).
6. Renal infarction.
7. Simple leukocyturia.
Examination
1. Blood tests
(1) Blood culture: taking venous blood for blood culture is the main basis for confirming the diagnosis of the disease, and it can also follow up whether the bacteremia persists. Especially cryptococcal and candidal infective endocarditis and prolonged infective endocarditis.
(2) General laboratory tests: Red blood cells and hemoglobin are decreased, and hemolysis may occur. Leukocytes are increased or normal, monocytes may be increased in classification, blood sedimentation is increased, serum gamma globulin is increased, IgG, IgM is increased, complement is decreased, and rheumatoid factor is positive.
(3) Serum immunologic examination.
2. Renal biopsy pathologic examination
In acute cases, the results only show neutrophilic leukocytes, monocyte infiltration, endothelial and thylakoid cells proliferation, while patients with subacute endocarditis may show diffuse damage to the glomeruli, with IgG, IgM and C3 deposits in the subepithelial, subendothelial, intrabasal membrane, and thylakoid areas, proliferation of intra- and extracellular cells in the capillaries, and glomerulosclerosis.
3.Echocardiography
It is valuable in diagnosing infective endocarditis and some of its intracardiac complications.
4 Imaging examination
Chest X-ray, computerized X-ray tomography CT or spiral CT, and magnetic resonance imaging (MRI) can clearly visualize the presence or absence of cardiac complications.
Diagnosis.
Diagnosis is based on:
1. patients with pre-existing heart valve damage or precordial heart, the production of a new murmur or a change in the pre-existing murmur, accompanied by the phenomenon of embolism, or persistent fever, anemia, splenomegaly, and blood cultures to bacteria.
2. The presence of hematuria, egg auturia, and tubular urine in those with the above conditions. Primary renal disease, urinary tract infection and long-term or recent right heart failure with depressed blood circulation can be excluded. No aminoglycoside antibiotics or nephrotoxic drugs were used before the urine examination. Removal of fever and menstrual abnormalities in female patients.
Treatment
1. Treatment of infective endocarditis
(1) Antibiotic treatment (preferred penicillin); the principle of antimicrobial use is that the drug should be used early; the choice of bactericidal drugs; the dose should be sufficient; the course of treatment should be long.
(2) Symptomatic supportive therapy.
(3) Anti-heart failure treatment.
(4) Anti-arrhythmic treatment.
(5) Heart valve replacement if necessary.
2. Treatment of kidney damage in infective endocarditis
Currently recognized effective antibiotics are sufficient to effectively treat mild renal damage caused by IE. However, IE causes severe diffuse nephritis, especially crescentic nephritis. There is no uniformity in the use of glucocorticoids or cytotoxic drugs. Antibiotics alone have been reported to result in complete recovery from IE-induced acute progressive nephritis. However, it has also been reported that patients on antibiotics alone end up with end-stage renal disease or death. Many scholars believe that surgery or plasma exchange can successfully treat acute progressive nephritis due to IE. There are more reports on glucocorticoids or immunosuppressive agents for the treatment of acute progressive nephritis due to IE, but the efficacy is not certain.