Infective endocarditis and kidney damage: symptoms

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 symptoms of infective endocarditis: fever, chills, night sweats, weakness, anorexia, weight loss, arthralgia, myalgia, splenomegaly.
  • Specific symptoms of infective endocarditis and damage to the valves: the appearance or change in the nature of 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.
  • Immunopathological manifestations: glomerulonephritis, myocarditis, polyarthritis, skin vasculitis (vascular purpura, Osler's nodules).

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

Renal damage

The defeat of the kidney in infectious endocarditis is diverse and can be associated with both the disease itself and the antibacterial drugs used for its treatment.

Renal damage in infectious endocarditis

Nature of the image	Cause of defeat
Kidney infarction	Thromboembolism from vegetation (branch of the renal artery)
	Immunopathological reactions (vasculitis of renal vessels)
Acute cortical necrosis	Thromboembolism (the trunk of the renal artery)
	Destruction of the valve with the development of acute heart failure
Abscess of the kidneys	Bacteremia with metastatic foci in organs
Glomerulonephritis	Immunopathological reactions
Amyloidosis	Chronic course of infective endocarditis
Drug nephropathy (acute interstitial nephritis, acute tubular necrosis)	Antibacterial drugs

Renal damage complicates the course of infective endocarditis in 50-80% of patients, and 10% of them develop chronic renal failure. The most common variant of kidney damage, in some cases, determining the prognosis, is glomerulonephritis, which occurs with infective endocarditis in 20-25% of cases. The connection between glomerulonephritis and infective endocarditis was first noticed by M. Lohlein, who in 1910 described focal glomerular changes, which he regarded as manifestations of "bacterial embolism" in a patient who died of infectious endocarditis. Already in 1932, A. Bell questioned the embolic nature of glomerulonephritis in infective endocarditis and suggested the leading role of immune mechanisms in the development of kidney damage. At present, the immune nature of the glomerular lesion is undoubted and is confirmed by the development of glomerulonephritis in endocarditis of the right heart, when embolism in the kidney vessels, the presence of hypocomplexemia, the detection of circulating and fixed immune complexes in the glomeruli, as well as specific bacterial antigens in their composition.

The main symptoms of glomerulonephritis in infectious endocarditis are hematuria, often reaching the degree of macrogematuria, and proteinuria. Nephrotic syndrome develops in 30-50% of patients, arterial hypertension is not typical. In some patients, kidney damage manifests with acute nephritic syndrome or increasing renal failure due to the development of rapidly progressing glomerulonephritis. In rare cases, the symptoms of kidney damage can precede the unfolded clinical picture of endocarditis ("nephritic" mask of infective endocarditis).

According to the spectrum of clinical manifestations and the morphological pattern, glomerulonurfrit in infectious endocarditis is similar to shunt-nephritis, a post-infection glomerulon-erfrit that develops in patients with an infected ventriculo-atrial shunt (connects the ventricle of the brain to the right atrium) established to eliminate occlusive hydrocephalus. In 80% of the cases, the causative agent of the "shunt infection" is epidermal staphylococcus, colonizing the distal (atrial) part of the shunting system either at the time of surgery to install it, or, more often, as a result of transient bacteremia, in the same way as with endocardial infection in infective endocarditis . Renal manifestation of "shunt jade" is usually preceded by a clinical picture of subacute sepsis with episodes of fever, malaise, anemia, splenomegaly. Most patients experience symptoms of intracranial hypertension (headaches, nausea, vomiting, drowsiness) due to dysfunction of the shunt associated with infection. Patients with a "shunt infection" also develop systemic manifestations (arthritis, cutaneous necrotizing vasculitis). The most common renal manifestations of "shunt jade" are hematuria (macrogemaria in a third of patients) and proteinuria. Nephrotic syndrome and arterial hypertension occur in about half of cases, renal dysfunction in 60%. In recent years, there has been a trend towards transformation of both clinical and morphological picture of "shunt jade": more and more often with kidney biopsy, extracapillary glomerulonerfrit with semilunas is detected with prevalence of clinical symptoms of fast-acting glomerulonephritis. The main reason for the progression of "shunt jade" is the long persistence of the infection, associated mainly with the untimely established diagnosis.