Symptomatic Anti-Neutrophil Cytoplasmic Antibody-Positive Disease Complicating Subacute Bacterial Endocarditis: To Treat or Not to Treat?

Konstantinov, Konstantin N.; Harris, Angela P.; Hartshorne, Michael F.; Tzamaloukas, Antonios H.

doi:10.1159/000339409

Cited by 21 publications

(30 citation statements)

References 14 publications

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“…La literatura recoge 16 casos de ANCA positivos en pacientes con endocarditis y glomerulonefritis aguda en biopsia renal (Tabla 1), de los cuales diez son ANCA anti-PR3 positivos [5][6][7][8][9][10][11][12][13] , dos anti-mieloperoxidasa 11,14 y en cinco de ellos no se especifica el tipo [15][16][17][18][19] . Los ANCA anti-PR3 se pueden elevar en enfermedades del tejido conectivo e infecciones crónicas como endocarditis subagudas bacterianas, tuberculosis o infección por el virus de la hepatitis B o C 5 , así como en ancianos.…”

Section: Discussionunclassified

Glomerulonefritis rápidamente progresiva asociada a endocarditis afebril y anca anti-proteinasa 3

Rodriguez

Zambrano

Cadiñanos

et al. 2017

Rev. Colomb. Nefrol.

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Resumen La endocarditis asociada a ANCA anti-PR3 e insuficiencia renal plantea un dilema tanto en su diagnóstico como tratamiento. Para abordar una revisión de dicho tema, se presenta el caso de un paciente con glomerulonefritis rápidamente progresiva secundaria a endocarditis subaguda por Enterococcus faecalis y positividad para ANCA anti-PR3. El diagnóstico diferencial principal se establecería entre una afectación renal de una vasculitis asociada a ANCA no diagnosticada previamente vs una glomerulonefritis postinfecciosa secundaria a la endocarditis. En muchos casos es necesario disponer de una biopsia renal que esclarezca el diagnóstico, ya que una inmunofluorescencia negativa orientará hacia una vasculitis, mientras que una positividad para inmunocomplejos iría a favor de una glomerulonefritis postestreptocócica. El tratamiento a seguir es otro reto que se plantea en la coexistencia de insuficiencia renal aguda, endocarditis y ANCA anti-PR3 positivo. La positividad de ANCAs induce a valorar iniciar tratamiento con inmunosupresores, no obstante, en el lecho de una endocarditis puede resultar desaconsejado e incluso poner en riesgo la vida del paciente someterlo a un estado de inmunosupresión. Es, por tanto, controvertido el uso de inmunosupresión en combinación con antibioterapia en el proceso agudo en contraposición al uso de antibioterapia exclusivamente. En el actual artículo se recogen los 19 casos publicados en la literatura de endocarditis asociados a ANCA anti-PR3, así como el tratamiento que se realizó en cada uno de los casos y la evolución en la función renal de cada paciente, concluyendo, en general, una mejor recuperación de la función renal en los pacientes tratados con antibioterapia en exclusiva que en aquellos tratados con la combinación antibiótico-corticoides. Sin embargo, dado el pequeño tamaño muestral, no se puede considerar significativa la diferencia entre ambos tratamientos. Absctrat Endocarditis associated with antiPR3 ANCA and acute kidney injure generates a challenge in its diagnosis and treatment. In order to make a review about that combination, we presented a patient with necrotizing glomerulonephritis produced by a Enterococcus faecalis´s subacute endocarditis and antiPR3 ANCA positive. Differential diagnosis is made between an acute kidney failure produced by ANCA´s vasculitis vs necrotizing glomerulonephritis by endocarditis. Frequently it is necessary to make a biopsy to get a diagnosis. Negative immunofluorescence will guide to vasculitis associated ANCA, while positive immune complexes will guide to poststreptococcal glomerulonephritis. Other challenge that generates the association of acute kidney disease, endocarditis and antiPR3 ANCA is the treatment. ANCA positive can prompt to start immunosuppressant treatments. However, in the context of endocarditis, it could be inadvisable and even dangerous to use it. For this reason, it is controversial the use of immunosuppressant in combination with antibiotics in the acute process, in contrast with the use of only antibiotics....

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Section: Discussionunclassified

Glomerulonefritis rápidamente progresiva asociada a endocarditis afebril y anca anti-proteinasa 3

Rodriguez

Zambrano

Cadiñanos

et al. 2017

Rev. Colomb. Nefrol.

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“…The majority of the patients had positive c-ANCA and/or anti-PR3 serologies. Four patients had positive c-ANCA and elevated titers of both anti-PR3 and anti-MPO antibodies [36,48]. Two patients had elevated titers of all four ANCA antibodies [34].…”

Section: Laboratory Testsmentioning

confidence: 94%

“…Immunofluorescence findings were reported in 19 patients. Electron microscopy findings were reported in only four patients [29,44,48,50]. Table 9 shows the histological diagnoses of renal pathology.…”

Section: Renal Manifestationsmentioning

confidence: 99%

Renal Disease in Patients with Infective Endocarditis and Antineutrophil Cytoplasmic Antibodies

Konstantinov¹,

Reyes²,

Barry³

et al. 2013

Cureus

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Infective endocarditis triggers the development of multiple immunological reactions, including the formation of autoantibodies. Certain categories of autoantibodies triggered by endocarditis, for example, antineutrophil cytoplamic antibodies (ANCA), may cause secondary diseases that require special diagnostic approaches and at times special interventions. Formation of ANCA secondary to endocarditis has been linked to vasculitis and renal disease. To evaluate the characteristics of renal disease in patients with infective endocarditis developing ANCA, we reviewed the reports of this syndrome. Forty-eight patients with endocarditis and positive ANCA serology were identified. Renal manifestations, including hematuria, proteinuria, and various levels of decrease in glomerular filtration rate, were almost ubiquitous. Renal histology, available from percutaneous kidney biopsy or autopsy in 28 subjects, revealed various pictures, including tubular injury, acute interstitial nephritis, post-infectious glomerulonephritis, pauciimmune glomerulonephritis, and others. The histological characterization of the renal and other lesions, along with the clinical picture, influenced the methods of treatment. Treatment of the underlying infection with antibiotics was associated with substantial improvement of clinical and laboratory features in most patients. However, a small number of patients with ANCA-mediated renal disease required immunosuppressive medications (corticosteroids, cyclophosphamide) or plasma exchange, with prompt and sustained response to these treatments. Ten patients died as a consequence of the endocarditis and 20 patients had surgical cardiac interventions. Disease secondary to autoantibodies triggered by endocarditis may require immunosuppressive medications in addition to antibiotics. Use of immunosuppressives carries the risk of sepsis in a setting of established infection. Defining the histology of the renal lesion in patients with infective endocarditis, ANCA formation, and renal involvement is required to identify patients who can potentially profit from the addition of immunosuppressive medication to antibiotics.

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“…In a case series, PR3‐ANCA and associated small vessel vasculitis (SVV) developed in patients with infective endocarditis (IE) caused by Enterococcus faecalis , Streptococcus mutans , Streptococcus oralis and Bartonella henselae . It was concluded that with some infective agents, subacute and/or chronic inflammatory states including infective endocarditis, may induce formation of auto‐antibodies, such as ANCA, which may in turn carry some cross‐reactivity with immune components or endothelial cells, and yield vessel wall damage and vasculitis …”

Section: Pathogenesismentioning

confidence: 98%

“…Humoral and cellular immune response may also play a role in some forms of infection‐associated vasculitides. Increased production of IgA, IgA1 and impaired glycosylation of IgA1 have been reported in IgA vasculitis associated with C. difficile and M. pneumoniae , although the immune mechanisms leading to these changes have not been elucidated . In a case series, PR3‐ANCA and associated small vessel vasculitis (SVV) developed in patients with infective endocarditis (IE) caused by Enterococcus faecalis , Streptococcus mutans , Streptococcus oralis and Bartonella henselae .…”

Section: Pathogenesismentioning

confidence: 99%

Infection‐associated vasculitides

Haq

Pagnoux

2018

Int J of Rheum Dis

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Vasculitides are disorders characterized by inflammation of the vessel walls, often caused by autoimmunity, but sometimes as a result of microbial invasion. Almost all types of microbes including bacteria, viruses, protozoa and fungi have been incriminated in the pathogenesis of vasculitis. Accurate etiological diagnosis is important since immunosuppressive treatment may lead to further deterioration if infection is the cause of vasculitis. Clinical features sometimes provide clues to the etiology. Further evaluation requires a focused and cost-effective plan of laboratory investigation. The investigations aim at establishing the diagnosis of vasculitis and identify the causative organism. An accurate diagnosis of vasculitis optimally requires histological examination and imaging. For infection-associated vasculitis, the identification of the organism requires studies of stained specimens, cultures, and/or detection of antigens and antibodies. Ideally, the treatment involves administration of an appropriate antimicrobial. In non-self-limiting types of vasculitides, glucocorticoids are needed when the symptoms are progressive, with vital organs involvement, and sometimes, when there is no antimicrobial agent of proven efficacy against the incriminated agent. Additional immunosuppressive agents or interventions must be considered when the disease is severe and/or post-infective immune mechanisms are involved in the pathogenesis, e.g., severe HBV-or HCV-associated vasculitides. Available preventative vaccinations are also crucial. The incidence of HBV-associated vasculitides dramatically decreased following HBV vaccination campaigns, and other infection-associated vasculitides may as well in the future.

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Symptomatic Anti-Neutrophil Cytoplasmic Antibody-Positive Disease Complicating Subacute Bacterial Endocarditis: To Treat or Not to Treat?

Cited by 21 publications

References 14 publications

Glomerulonefritis rápidamente progresiva asociada a endocarditis afebril y anca anti-proteinasa 3

Glomerulonefritis rápidamente progresiva asociada a endocarditis afebril y anca anti-proteinasa 3

Renal Disease in Patients with Infective Endocarditis and Antineutrophil Cytoplasmic Antibodies

Infection‐associated vasculitides

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