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.
  • Non-specific symptoms of infective endocarditis: fever, chills, night sweats, weakness, anorexia, weight loss, arthralgia, myalgia, splenomegaly.
  • Specific symptoms of infective endocarditis and valve damage: the appearance or change in the nature of noises as a result of the formation of valve defects, perforation of the valves, rupture of the tendinous chords, rupture of the valve. These processes are complicated by the development of circulatory failure in more than 50% of patients.
  • Arterial embolisms of vegetation fragments: thromboembolism of cerebral vessels (acute cerebrovascular accident), myocardial infarction, pulmonary embolism, occlusion of mesenteric arteries with the development of an “acute abdomen” picture, splenic infarction, renal infarction, occlusion of large peripheral arteries (gangrene of the limb).
  • 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, cutaneous vasculitis (vascular purpura, Osler's nodes).

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

Kidney damage

Kidney damage in infective endocarditis varies widely and can be associated with both the disease itself and the antibacterial drugs used to treat it.

Kidney damage in infective endocarditis

The nature of the image	Reason for defeat
Renal infarction	Thromboembolism from vegetation (branches of renal artery)
	Immunopathological reactions (renal vasculitis)
Acute cortical necrosis	Thromboembolism (renal artery trunk)
	Valve destruction with development of acute heart failure
Kidney abscesses	Bacteremia with metastatic foci in organs
Glomerulonephritis	Immunopathological reactions
Amyloidosis	Chronic course of infective endocarditis
Drug-induced nephropathy (acute interstitial nephritis, acute tubular necrosis)	Antibacterial drugs

Kidney damage complicates the course of infective endocarditis in 50-80% of patients, with 10% of them developing chronic renal failure. The most common type of kidney damage, in some cases determining the prognosis, is glomerulonephritis, which occurs in 20-25% of cases of infective endocarditis. The connection between glomerulonephritis and infective endocarditis was first noted by M. Lohlein, who in 1910 described focal glomerular changes, which he regarded as manifestations of "bacterial embolism", in a patient who died from infective endocarditis. As early as 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. Currently, the immune nature of glomerular damage is beyond doubt and is confirmed by the development of glomerulonephritis in endocarditis of the right heart, when embolism in the renal vessels is excluded, the presence of hypocomplementemia, the detection of circulating and fixed immune complexes in the glomeruli in patients with infective endocarditis, as well as specific bacterial antigens in their composition.

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

In terms of the spectrum of clinical manifestations and morphological picture, glomerulonephritis in infective endocarditis is similar to "shunt nephritis" - post-infectious glomerulonephritis, which develops in patients with an infected ventriculoatrial shunt (connects the cerebral ventricle with the right atrium), installed to eliminate occlusive hydrocephalus. In 80% of cases, the causative agent of "shunt infection" is epidermal staphylococcus, colonizing the distal (atrial) part of the shunt system either at the time of surgery to install it, or, more often, as a result of transient bacteremia, similar to how it occurs with endocardial infection in infective endocarditis. Renal manifestation of "shunt nephritis" is usually preceded by a clinical picture of subacute sepsis with episodes of fever, malaise, anemia, splenomegaly. Most patients have symptoms of intracranial hypertension (headaches, nausea, vomiting, drowsiness) due to shunt dysfunction associated with its infection. Patients with "shunt infection" also develop systemic manifestations (arthritis, cutaneous necrotizing vasculitis). The most common renal manifestations of "shunt nephritis" are hematuria (macrohematuria in a third of patients) and proteinuria. Nephrotic syndrome and arterial hypertension occur in about half of cases, and renal dysfunction in 60%. In recent years, a tendency toward transformation of both the clinical and morphological picture of "shunt nephritis" has been noted: increasingly, kidney biopsy reveals extracapillary glomerulonephritis with crescents with a predominance of clinical symptoms of rapidly progressive glomerulonephritis. The main reason for the progression of shunt nephritis is considered to be the long-term persistence of infection, associated mainly with an untimely diagnosis.