To identify differences in treatment and outcome of various types of glomerulonephritis developing in the course of infections triggering antineutrophil cytoplasmic antibody (ANCA) formation, we analyzed published reports of 50 patients. Immunosuppressives were added to antibiotics in 22 of 23 patients with pauci-immune glomerulonephritis. Improvement was noted in 85% of 20 patients with information on outcomes. Death rate was 13%. Corticosteroids were added to antibiotics in about 50% of 19 patients with postinfectious glomerulonephritis. Improvement rate was 74%, and death rate was 26%. Two patients with mixed histological features were analyzed under both pauci-immune and post-infectious glomerulonephritis categories. In 9 patients with other renal histology, treatment consisted of antibiotics alone (7 patients), antibiotics plus immunosuppressives (1 patient), or immunosuppressives alone (1 patient). Improvement rate was 67%, permanent renal failure rate was 22%, and death rate was 11%. One patient with antiglomerular basement disease glomerulonephritis required maintenance hemodialysis. Glomerulonephritis developing in patients who became ANCA-positive during the course of an infection is associated with significant mortality. The histological type of the glomerulonephritis guides the choice of treatment. Pauci-immune glomerulonephritis is usually treated with addition of immunosuppressives to antibiotics. 1. Introduction The reaction of the body to infections may cause secondary illnesses, such as rheumatic fever and poststreptococcal glomerulonephritis, with potentially life-threatening manifestations. An early step in the research to unravel the link between infection and secondary illness was the discovery that chronic infections trigger multiple immunological responses potentially associated with specific diseases [1]. Infections can lead to formation of multiple autoantibodies, for example, rheumatoid factor, antinuclear antibodies (ANAs), antiphospholipid antibodies, and antineutrophil cytoplasmic antibodies (ANCAs). The development of autoantibodies in the course of an infection may or may not be associated with manifestations of autoimmune disease. The recognition of autoimmune manifestations during the course of an infection and the decision to add specific treatment for the secondary immunological abnormality or to treat only the infection and monitor the patient for attenuation and disappearance of the immunological manifestations are critical tasks. The search for organ manifestations that can help the distinction between infectious
References
[1]
R. C. Williams Jr. and H. G. Kunkel, “Rheumatoid factor, complement, and conglutinin aberrations in patients with subacute bacterial endocarditis,” The Journal of Clinical Investigation, vol. 41, pp. 666–675, 1962.
[2]
M. Lohlein, “Ueber haemorrhagische nierenaffectionen bei chronischer ulcerozer endocarditis,” Medicinische Klinik, vol. 10, pp. 375–379, 1910.
[3]
K. Lange, G. Seligson, and W. Cronin, “Evidence for the in situ origin of poststreptococcal glomerulonephritis: glomerular localization of endostreptosin and the clinical significance of the subsequent antibody response,” Clinical Nephrology, vol. 19, no. 1, pp. 3–10, 1983.
[4]
A. S. Bayer, A. N. Theofilopoulos, and R. Eisenberg, “Circulating immune complexes in infective endocarditis,” New England Journal of Medicine, vol. 295, no. 27, pp. 1500–1505, 1976.
[5]
F. J. Dixon, J. D. Feldman, and J. J. Vasquez, “Experimental glomerulonephritis: the pathogenesis of a laboratory model resembling the spectrum of human glomerulonephritis,” Journal of Experimental Medicine, vol. 113, pp. 899–920, 1961.
[6]
R. A. Gutman, G. E. Striker, B. C. Gilliland, and R. E. Cutler, “The immune complex glomerulonephritis of bacterial endocarditis,” Medicine, vol. 51, no. 1, pp. 1–25, 1972.
[7]
W. G. Couser, “Mechanisms of glomerular injury in immune-complex disease,” Kidney International, vol. 28, no. 3, pp. 569–583, 1985.
[8]
G. O. Perez, N. Rothfield, and R. C. Williams, “Immune complex nephritis in bacterial endocarditis,” Archives of Internal Medicine, vol. 136, no. 3, pp. 334–336, 1976.
[9]
R. L. Levy and R. Hong, “The immune nature of subacute bacterial endocarditis (SBE) nephritis,” The American Journal of Medicine, vol. 54, no. 5, pp. 645–652, 1973.
[10]
H. K. Choi, P. A. Merkel, A. M. Walker, and J. L. Niles, “Drug-associated antineutrophil cytoplasmic antibody-positive vasculitis,” Arthritis & Rheumatism, vol. 43, pp. 405–413, 2000.
[11]
H. H. Peter, D. Metzger, A. Rump, and E. Rother, “ANCA in diseases other than systemic vasculitis,” Clinical and Experimental Immunology, vol. 93, no. 1, supplement, pp. 12–14, 1993.
[12]
L. Nassberger, A. G. Sjoholm, H. Jonsson, G. Sturfelt, and A. Akesson, “Autoantibodies against neutrophil cytoplasm components in systemic lupus erythematosus and in hydralazine-induced lupus,” Clinical and Experimental Immunology, vol. 81, no. 3, pp. 380–383, 1990.
[13]
N. Makita, H. Katori, F. Takemoto et al., “A case of mixed connective tissue disease (MCTD) complicated with MPO-ANCA-related necrotizincj gloomerulonephritis,” Clinical Nephrology, vol. 54, no. 2, pp. 164–168, 2000.
[14]
D. Bansi, R. W. Chapman, and K. Fleming, “Antineutrophil cytoplasmic antibodies in chronic liver diseases: prevalence, titre, specificity and IgG subclass,” Journal of Hepatology, vol. 24, no. 5, pp. 581–586, 1996.
[15]
R. H. Duerr, S. R. Targan, C. J. Landers et al., “Neutrophil cytoplasmic antibodies: a link between primary sclerosing cholangitis and ulcerative colitis,” Gastroenterology, vol. 100, no. 5 I, pp. 1385–1391, 1991.
[16]
D. Zauli, S. Ghetti, A. Grassi et al., “Anti-neutrophilcytoplasmic antibodies in type 1 and 2 autoimmune hepatitis,” Hepatology, vol. 25, no. 5, pp. 1105–1107, 1997.
[17]
Y. Hosoya, S. Minota, A. Lefor et al., “Resolution of anti-neutrophil cytoplasmic antibody-associated vasculitis after resection of gastric cancer,” Modern Rheumatology, vol. 20, no. 1, pp. 102–105, 2010.
[18]
T. Cil, A. Altintas, A. Isikdogan, and S. Batun, “Prevalence of antineutrophil cytoplasmic antibody positivity in patients with Hodgkin's and non-Hodgkin lymphoma: a single center experience,” International Journal of Hematology, vol. 90, no. 1, pp. 52–57, 2009.
[19]
K. Tsuruoka, S. Sekiya, T. Yokoyama et al., “MPO-ANCA related vasculitis complicating mucinous cystadenoma of the pancreas and severe acute pancreatitis after steroid pulse therapy: a case report,” Japanese Journal of Nephrology, vol. 50, no. 7, pp. 948–953, 2008.
[20]
M. Wong, J. Grossman, B. H. Hahn, and A. La Cava, “Cutaneous vasculitis in breast cancer treated with chemotherapy,” Clinical Immunology, vol. 129, no. 1, pp. 3–9, 2008.
[21]
J. G. Parambil, K. A. Keogh, F. C. Fervenza, and J. H. Ryu, “Microscopic polyangiitis associated with thymoma, exacerbating after thymectomy,” American Journal of Kidney Diseases, vol. 48, no. 5, pp. 827–831, 2006.
[22]
S. D. Navaneethan, J. Taylor, B. Goldman, and A. Bose, “Anti-neutrophil cytoplasmic antibody associated crescentic IgA nephropathy in hematopoietic stem cell transplantation,” Clinical Nephrology, vol. 71, no. 1, pp. 59–62, 2009.
[23]
B. Terjung and U. Spengler, “Atypical p-ANCA in PSC and AIH: a hint toward a “leaky gut”?” Clinical Reviews in Allergy and Immunology, vol. 36, no. 1, pp. 40–51, 2009.
[24]
Y. Wada, T. Kuroda, A. Murasawa, M. Nakano, and I. Narita, “Anti-neutrophil cytoplasmic autoantibodies against bactericidal/permeability-increasing protein in patients with rheumatoid arthritis and their correlation with bronchial involvement,” Modern Rheumatology, vol. 20, no. 3, pp. 252–256, 2010.
[25]
L. Harper and C. O. Savage, “ANCA-associated renal vasculitis at the end of the twentieth century—a disease of older patients,” Rheumatology, vol. 44, no. 4, pp. 495–501, 2005.
[26]
C. A. Langford, “Cyclophosphamide as induction therapy for Wegener's granulomatosis and microscopic polyangiitis,” Clinical and Experimental Immunology, vol. 164, no. 1, supplement, pp. 31–34, 2011.
[27]
F. Rees, R. Yazdani, and P. Lanyon, “Long-term follow-up of different refractory systemic vasculitides treated with rituximab,” Clinical Rheumatology, vol. 30, pp. 1241–1245, 2011.
[28]
A. Majumdar, S. Chowdhary, M. A. S. Ferreira et al., “Renal pathological findings in infective endocarditis,” Nephrology Dialysis Transplantation, vol. 15, no. 11, pp. 1782–1787, 2000.
[29]
J. I. Zeledon, R. L. McKelvey, K. S. Servilla et al., “Histological varieties and treatment of glomerulonephritis causing acute renal failure during the course of bacterial infections,” International Urology and Nephrology, vol. 40, no. 2, pp. 461–470, 2008.
[30]
R. J. L. Klaassen, R. Goldschmeding, K. M. Dolman et al., “Anti-neutrophil cytoplasmic autoantibodies in patients with symptomatic HIV infection,” Clinical and Experimental Immunology, vol. 87, no. 1, pp. 24–30, 1992.
[31]
F. Bonnet, J. J. Pineau, J. L. Taupin et al., “Prevalence of cryoglobulinemia and serological markers of autoimmunity in human immunodeficiency virus infected individuals: a cross-sectional study of 97 patients,” Journal of Rheumatology, vol. 30, no. 9, pp. 2005–2010, 2003.
[32]
L. H. Calabrese, “Infection with the human immunodeficiency virus type 1 and vascular inflammatory disease,” Clinical and Experimental Rheumatology, vol. 22, no. 6, pp. S87–S93, 2004.
[33]
A. Kamat, P. Ancuta, R. S. Blumberg, and D. Gabuzda, “Serological markers for inflammatory bowel disease in aids patients with evidence of microbial translocation,” PLoS ONE, vol. 5, no. 11, Article ID e15533, 2010.
[34]
H. K. Choi, P. Lambrecht, K. L. Niles, W. L. Gross, and P. A. Merkel, “Subacute bacterial endocarditis with positive antineutrophil cytoplasmic antibodies and anti-proteinase 3 antibodies,” Arthritis & Rheumatism, vol. 43, pp. 226–231, 2000.
[35]
A. De Corla-Souza and B. A. Cunha, “Streptococcal viridans subacute bacterial endocarditis associated with antineutrophil cytoplasmic autoantibodies (ANCA),” Heart and Lung, vol. 32, no. 2, pp. 140–143, 2003.
[36]
B. Bonaci-Nikolic, S. Andrejevic, M. Pavlovic, Z. Dimcic, B. Ivanovic, and M. Nikolic, “Prolonged infections associated with antineutrophil cytoplasmic antibodies specific to proteinase 3 and myeloperoxidase: diagnostic and therapeutic challenge,” Clinical Rheumatology, vol. 29, no. 8, pp. 893–904, 2010.
[37]
L. Guillevin, H. Visser, F. Oksman, and J. Pourrat, “Antineutrophil cytoplasmic antibodies in polyarteritis nodosa related to hepatitis B virus,” Arthritis and Rheumatism, vol. 33, no. 12, pp. 1871–1872, 1990.
[38]
L. Guillevin, H. Visser, L. H. Noel et al., “Antineutrophil cytoplasm antibodies in systemic polyarteritis nodosa with and without hepatitis B virus infection and Churg-Strauss syndrome—62 patients,” Journal of Rheumatology, vol. 20, no. 8, pp. 1345–1349, 1993.
[39]
R. Kasmani, K. Okoli, K. Naraharisetty, W. Gunning, J. I. Shapiro, and S. Ratnam, “Microscopic polyangiitis triggered by recurrent methicillin-resistant Staphylococcus aureus bacteremia,” International Urology and Nephrology, vol. 42, no. 3, pp. 821–824, 2010.
[40]
S. P. McAdoo, C. Densem, A. Salama, and C. D. Pusey, “Bacterial endocarditis associated with proteinase 3 anti-neutrophil cytoplasm antibody,” NDT Plus, vol. 4, no. 3, pp. 208–210, 2011.
[41]
J. Romani, L. Puig, and J. N. De Moragas, “Detection of antineutrophil cytoplasmic antibodies in patients with hepatitis C virus-induced cutaneous vasculitis with mixed cryoglobulinemia,” Archives of Dermatology, vol. 132, no. 8, pp. 974–975, 1996.
[42]
H. Ohira, J. Tojo, J. Shinzawa et al., “Antineutrophil cytoplasmic antibody in patients with antinuclear antibody-positive chronic hepatitis C,” Fukushima Journal of Medical Science, vol. 44, no. 2, pp. 83–92, 1998.
[43]
P. Lamprecht, O. Gutzeit, E. Csernok et al., “Prevalence of ANCA in mixed cryoglobulinemia and chronic hepatitis C virus infection,” Clinical and Experimental Rheumatology, vol. 21, no. 6, pp. S89–S94, 2003.
[44]
M. Cojocaru, I. M. Cojocaru, and S. A. Iacob, “Prevalence of anti-neutrophil cytoplasmic antibodies in patients with chronic hepatitis C infection associated mixed cryoglobulinemia,” Romanian Journal of Internal Medicine, vol. 44, no. 4, pp. 427–431, 2006.
[45]
T. N. K. Chou, T. C. Hsu, R. M. Chen, L. I. Lin, and G. J. Tsay, “Parvovirus B19 infection associated with the production of antineutrophil cytoplasmic antibody (ANCA) and anticardiolipin antibody (aCL),” Lupus, vol. 9, no. 7, pp. 551–554, 2000.
[46]
J. Hermann, U. Demel, D. Stünzner, E. Daghofer, G. Tilz, and W. Graninger, “Clinical interpretation of antineutrophil cytoplasmic antibodies: parvovirus B19 infection as a pitfall,” Annals of the Rheumatic Diseases, vol. 64, no. 4, pp. 641–643, 2005.
[47]
C. M. Magro, R. Wusirika, G. E. Frambach, G. J. Nuovo, C. Ferri, and P. Ross, “Autoimmune-like pulmonary disease in association with parvovirus B19: a clinical, morphologic, and molecular study of 12 cases,” Applied Immunohistochemistry and Molecular Morphology, vol. 14, no. 2, pp. 208–216, 2006.
[48]
P. von Landenberg, H. W. Lehmann, and S. Modrow, “Human parvovirus B19 infection and antiphospholipid antibodies,” Autoimmunity Reviews, vol. 6, no. 5, pp. 278–285, 2007.
[49]
K. Satake, I. Ohsawa, N. Kobayashi et al., “Three cases of PR3-ANCA positive subacute bacterial endocarditis caused by attenuated bacteria (Propionibacterium, Gemella, and Bartonella) complicated with kidney injury,” Modern Rheumatology, vol. 21, pp. 536–541, 2011.
[50]
D. J. Davies, J. E. Moran, J. F. Niall, and G. B. Ryan, “Segmental necrotising glomerulonephritis with antineutrophil antibody: possible arbovirus aetiology?” British Medical Journal, vol. 285, no. 6342, article 606, 1982.
[51]
A. Bauer, W. J. Jabs, S. Süfke, M. Maass, and B. Kreft, “Vasculitic purpura with antineutrophil cytoplasmic antibody-positive acute renal failure in a patient with Streptococcus bovis and Neisseria subflava bacteremia and subacute endocarditis,” Clinical Nephrology, vol. 62, no. 2, pp. 144–148, 2004.
[52]
A. Steitz, T. Orth, A. Feddersen, T. Fischer, E. Marker-Hermann, and M. Husmann, “A case of endocarditis with vasculitis due to Actinobacillus actinomycetemcomitans: a 16S rDNA signature for distinction from related organisms,” Clinical Infectious Diseases, vol. 27, no. 1, pp. 224–225, 1998.
[53]
R. Mahadeva, A. C. Dunn, R. C. Westerbeek et al., “Anti-neutrophil cytoplasmic antibodies (ANCA) against bactericidal/permeability-increasing protein (BPI) and cystic fibrosis lung disease,” Clinical and Experimental Immunology, vol. 117, no. 3, pp. 561–567, 1999.
[54]
E. Carmona, F. Perez-Aguilar, J. A. Lopez, J. Ferrer-Calvete, and J. M. Sanchez-Cuenca, “Anti-neutrophil-cytoplasmic auto-antibodies (ANCA) in 105 patients (56 adults and 49 children) suffering from cystic fibrosis, attending a Spanish hospital,” Journal of Internal Medicine, vol. 252, no. 3, pp. 281–282, 2002.
[55]
L. Dorl？chter, M. Carlsson, E. J. Olafsdottir, O. D. Ro？ksund, K. Rosendahl, and G. Fluge, “Anti-neutrophil cytoplasmatic antibodies and lung disease in cystic fibrosis,” Journal of Cystic Fibrosis, vol. 3, no. 3, pp. 179–183, 2004.
[56]
M. Rotschild, N. Elias, D. Berkowitz et al., “Autoantibodies against bactericidal/permeability-increasing protein (BPI-ANCA) in cystic fibrosis patients treated with azithromycin,” Clinical and Experimental Medicine, vol. 5, no. 2, pp. 80–85, 2005.
[57]
O. Cohavy, D. Bruckner, L. K. Gordon et al., “Colonic bacteria express an ulcerative colitis pANCA-related protein epitope,” Infection and Immunity, vol. 68, no. 3, pp. 1542–1548, 2000.
[58]
H. Locht, E. Peen, and T. Skogh, “Antineutrophil cytoplasmic antibodies in reactive arthritis,” Journal of Rheumatology, vol. 22, no. 12, pp. 2304–2306, 1995.
[59]
K. Zycinska, K. A. Wardyn, Z. Zycinski, and R. Smolarczyk, “Correlation between Helicobacter pylori infection and pulmonary wegener's granulomatosis activity,” Journal of Physiology and Pharmacology, vol. 59, no. 6, pp. 845–851, 2008.
[60]
H. Schultz, E. Csernok, S. Nikkari, P. Toivanen, A. Toivanen, and W. L. Gross, “BPI-ANCA is found in reactive arthritis caused by Yersinia and Salmonella infection and recognise exclusively the C-terminal part of the BPI molecule,” Scandinavian Journal of Rheumatology, vol. 29, no. 4, pp. 226–231, 2000.
[61]
C. Bechara, M. Gousseff, A. Passeron et al., “Corynebacterium jeikeium pacemaker infection associated with antineutrophil cytoplasmic antibodies: a single positive blood culture could be sufficient for diagnosis,” Journal of Medical Microbiology, vol. 60, no. 2, pp. 249–251, 2011.
[62]
J. Park, S. Banno, Y. Sugiura et al., “Microscopic polyangiitis associated with diffuse panbronchiolitis,” Internal Medicine, vol. 43, no. 4, pp. 331–335, 2004.
[63]
E. K. Bell, S. S. Chugh, and W. J. Cook, “A case of infection-associated antiproteinase-3-negative cytoplasmic antineutrophil cytoplasmic antibody pauci-immune focal necrotizing glomerulonephritis,” Nephrology Dialysis Transplantation, vol. 25, no. 9, pp. 3119–3123, 2010.
[64]
K. Trcko, P. B. Marko, and J. Milijkovic, “Leucocytoclastic vasculitis induced by Mycoplasma pneumoniae infection,” Acta Dermatovenerologica Croatica, vol. 20, pp. 118–121, 2012.
[65]
M. Iyoda, T. Hato, K. Matsumoto et al., “Rapidly progressive glomerulonephritis in a patient with Chlamydia pneumoniae infection: a possibility of superantigenic mechanism of its pathogenesis,” Clinical Nephrology, vol. 65, no. 1, pp. 48–52, 2006.
[66]
M. Iyoda, A. Kuroki, and T. Sugisaki, “Chlamydia pneumoniae infection and MPO-ANCA-associated glomerulonephritis,” Nephrology Dialysis Transplantation, vol. 22, no. 3, pp. 965–966, 2007.
[67]
M. Fujita, S. Hatachi, and M. Yagita, “Acute Chlamydia pneumoniae infection in the pathogenesis of autoimmune diseases,” Lupus, vol. 18, no. 2, pp. 164–168, 2009.
[68]
G. Cabiddu, P. Altieri, A. Pani et al., “Mediterranean spotted fever with acute renal failure simulating a relapse in C-ANCA vasculitis,” Nephron, vol. 79, no. 2, pp. 241–242, 1998.
[69]
A. Garcia-Zamalloa, N. Gurruchaga, and M. Montes, “Q fever and antineutrophil cytoplasmic antibodies,” American Journal of Medicine, vol. 108, no. 8, pp. 687–688, 2000.
[70]
R. O. Holmes Jr., J. D. Hartzell, J. K. Tofferi, J. D. Roebuck, and W. F. Kelly, “Dual high titer antineutrophil cytoplasmic autoantibodies in association with systemic Q fever,” Journal of Clinical Rheumatology, vol. 15, no. 8, pp. 411–413, 2009.
[71]
W. W？ckel, K. H？u？inger, R. Weis, and A. Morresi-Hauf, “Anticytoplasmatic antibody (cANCA) in syphilitic gumma of the lung,” Deutsche Medizinische Wochenschrift, vol. 121, no. 19, pp. 617–621, 1996.
[72]
A. Constantin, F. Marin, F. Oksman, and G. Bouteiller, “Antineutrophil cytoplasmic antibodies in leptospirosis,” The Journal of Rheumatology, vol. 23, no. 2, article 411, 1996.
[73]
B. F. A. Freire, A. A. F. Ferraz, E. Nakayama, S. Ura, and T. T. Queluz, “Anti-neutrophil cytoplasmic antibodies (ANCA) in the clinical forms of leprosy,” International Journal of Leprosy, vol. 66, no. 4, pp. 475–482, 1998.
[74]
F. Medina, A. Camargo, J. Moreno, A. Zonana-Nacach, J. Aceves-Avila, and A. Fraga, “Anti-neutrophil cytoplasmic autoantibodies in leprosy,” British Journal of Rheumatology, vol. 37, no. 3, pp. 270–273, 1998.
[75]
O. Cohavy, G. Harth, M. Horwitz et al., “Identification of a novel mycobacterial histone H1 homologue (HupB) as an antigenic target of pANCA monoclonal antibody and serum immunoglobulin A from patients with Crohn's disease,” Infection and Immunity, vol. 67, no. 12, pp. 6510–6517, 1999.
[76]
V. D. Pradhan, S. S. Badakere, K. Ghosh, and A. R. Pawar, “Spectrum of anti-neutrophil cytoplasmic antibodies in patients with Pulmonary Tuberculosis overlaps with that of Wegener's granulomatosis,” Indian Journal of Medical Sciences, vol. 58, no. 7, pp. 283–288, 2004.
[77]
S. Chaiamnuay and L. W. Heck, “Antineutrophil cytoplasmic antibody vasculitis associated with Mycobacterium avium intracellulare infection,” Journal of Rheumatology, vol. 32, no. 8, pp. 1610–1612, 2005.
[78]
F. L. B. Edington, M. O. A. R. Bacellar, P. R. Machado et al., “Anti-neutrophil cytoplasmic antibodies in leprosy,” Clinical Rheumatology, vol. 26, no. 2, pp. 208–210, 2007.
[79]
S. Faruqi, J. A. Kastelik, and D. V. McGivern, “Diagnostic pitfall: Mycobacterium avium complex pulmonary infection and positive ANCA,” European Journal of Internal Medicine, vol. 19, no. 3, pp. 216–218, 2008.
[80]
K. Ghosh, V. Pradhan, and K. Ghosh, “Background noise of infection for using ANCA as a diagnostic tool for vasculitis in tropical and developing countries,” Parasitology Research, vol. 102, no. 5, pp. 1093–1095, 2008.
[81]
R. Sherkat, K. Mostafavizadeh, L. Zeydabadi, P. Shoaei, and S. Rostani, “Antineutrophil cytoplasmic antibodies in patients with pulmonary tuberculosis,” Iranian Journal of Immunology, vol. 8, pp. 52–57, 2011.
[82]
M. Kontic, S. Radovanovic, M. Nicolic, and B. Bonaci-Nicolic, “Concomitant drug- and infection-induced antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis with multispecific ANCA,” Medical Practice, vol. 21, pp. 488–491, 2012.
[83]
A. M. Milesi-Lecat, O. Aumaitre, T. Deusebis et al., “Semi-invasive pulmonary aspergillosis with anti-neutrophil cytoplasmic auto-antibodies: two cases,” Annales de Medecine Interne, vol. 145, no. 2, pp. 140–146, 1994.
[84]
C. Cho, A. Asuncion, and A. H. Tatum, “False-positive antineutrophil cytoplasmic antibody in aspergillosis with oxalosis,” Archives of Pathology and Laboratory Medicine, vol. 119, no. 6, pp. 558–561, 1995.
[85]
T. Akimoto, O. Saito, M. Inoue et al., “Rapid formation of Aspergillus mycetoma in a patient receiving corticosteroid treatment. Serial radiographic observation over two months,” Internal Medicine, vol. 46, no. 11, pp. 733–738, 2007.
[86]
T. Saito, N. Shime, K. Itoh et al., “Disseminated aspergillosis following resolution of Pneumocystis pneumonia with sustained elevation of beta-glucan in an intensive care unit: a case report,” Infection, vol. 37, no. 6, pp. 547–550, 2009.
[87]
G. E. Mead, D. Wilks, K. McLaren, and R. J. Fergusson, “Oral histoplasmosis: a case report,” Journal of Infection, vol. 37, no. 1, pp. 73–75, 1998.
[88]
R. P. Byrd, J. Hourany, C. Cooper, and T. M. Roy, “False-positive antineutrophil cytoplasmic antibodies in a patient with cavitary pulmonary sporotrichosis,” American Journal of Medicine, vol. 104, no. 1, pp. 101–103, 1998.
[89]
R. H. Evans, C. Gelder M, A. P. Smith, and A. R. Freedman, “Pneumocystis carinii pneumonia mimicking Wegener's granulomatosis,” Clinical Infectious Diseases, vol. 28, no. 5, pp. 1163–1164, 1999.
[90]
N. Takeda, H. Ichiyasu, A. Kijima, D. Notsute, N. Saita, and H. Kohrogi, “A case of AIDS with Pneumocystis jirovecii pneumonia which required differentiation from ANCA-related lung disease,” Nihon Kokyuki Gakkai Zasshi, vol. 49, pp. 929–935, 2011.
[91]
I. Stappaerts, J. Bogers, D. Ebo, E. Vanden Broecke, W. J. Stevens, and P. Vermeire, “c-ANCA positivity in a Belgian patient with pulmonary paracoccidioidomycosis,” European Respiratory Journal, vol. 10, no. 10, pp. 2419–2422, 1997.
[92]
C. Hartman, R. Eliakim, and R. Shamir, “Perinuclear antineutrophil cytoplasmic autoantibodies and anti-Saccharomyces cerevisiae antibodies: serologic markers in inflammatory bowel disease,” Israel Medical Association Journal, vol. 6, no. 4, pp. 221–226, 2004.
[93]
G. E. Reese, V. A. Constantinides, C. Simillis et al., “Diagnostic precision of anti-Saccharomyces cerevisiae antibodies and perinuclear antineutrophil cytoplasmic antibodies in inflammatory bowel disease,” American Journal of Gastroenterology, vol. 101, no. 10, pp. 2410–2422, 2006.
[94]
D. J. Pudifin, J. Duursma, V. Gathiram, and T. F. H. G. Jackson, “Invasive amoebiasis is associated with the development of anti-neutrophil cytoplasmic antibody,” Clinical and Experimental Immunology, vol. 97, no. 1, pp. 48–51, 1994.
[95]
S. Arslan, A. Bakkaloglu, G. Oksuzoglu et al., “The value of p-ANCA as a serological marker in diagnosing the coexistence of chronic active invasive amebic colitis and ulcerative colitis,” American Journal of Gastroenterology, vol. 90, no. 12, pp. 2265–2266, 1995.
[96]
C. Wenisch, H. Wenisch, H. Bankl -C et al., “Detection of anti-neutrophil cytoplasmic antibodies after acute Plasmodium falciparum malaria,” Clinical and Diagnostic Laboratory Immunology, vol. 3, pp. 132–134, 1996.
[97]
T. M. Yahya, S. Benedict, A. Shalabi, and R. Bayoumi, “Anti-neutrophil cytoplasmic antibody (ANCA) in malaria is directed against cathepsin G,” Clinical and Experimental Immunology, vol. 110, no. 1, pp. 41–44, 1997.
[98]
V. Pradhan, S. S. Badakere, U. Shankarkumar, Y. S. Iyer, K. Ghosh, and D. Karnad, “Anti-neutrophil Cytoplasmic Antibodies (ANCA) in Malaria,” Indian Journal of Malariology, vol. 39, no. 3-4, pp. 51–59, 2002.
[99]
E. Brahn, D. A. Pegues, Q. Yao, and N. Craft, “Mucocutaneous leishmaniasis masquerading as wegener granulomatosis,” Journal of Clinical Rheumatology, vol. 16, no. 3, pp. 125–128, 2010.
[100]
F. G. De Rosa, A. Amoroso, A. Teggi et al., “Anti-neutrophil cytoplasmic antibodies in Echinococcus granulosus hydatid disease,” Human Immunology, vol. 62, no. 10, pp. 1122–1126, 2001.
[101]
M. Rajapurkar, U. Hegde, M. Rokhade, S. Gang, and K. Gohel, “Respiratory hyperinfection with Strongyloides stercoralis in a patient with renal failure,” Nature Clinical Practice Nephrology, vol. 3, no. 10, pp. 573–577, 2007.
[102]
S. Kaya, M. Demirci, E. Sesli Cetin et al., “Investigation of the presence of autoantibodies in patients with toxocariasis,” Mikrobiyoloji Bülteni, vol. 43, pp. 661–666, 2009.
[103]
J. Wagner, K. Andrassy, and E. Ritz, “Is vasculitis in subacute bacterial endocarditis associated with ANCA?” Lancet, vol. 337, no. 8744, pp. 799–800, 1991.
[104]
L. Couzi, D. Morel, C. Deminière, and P. Merville, “An unusual endocarditis-induced crescentic glomerulonephritis treated by plasmapheresis,” Clinical Nephrology, vol. 62, no. 6, pp. 461–465, 2004.
[105]
M. Fukuda, M. Motokawa, T. Usami et al., “PR3-ANCA-positive crescentic necrotizing glomerulonephritis accompanied by isolated pulmonic valve infective endocarditis, with reference to previous reports of renal pathology,” Clinical Nephrology, vol. 66, no. 3, pp. 202–209, 2006.
[106]
N. Kishimoto, Y. Mori, H. Yamahara et al., “Cytoplasmic antineutrophil cytoplasmic antibody positive pauci-immune glomerulonephritis associated with infectious endocarditis,” Clinical Nephrology, vol. 66, no. 6, pp. 447–454, 2006.
[107]
K. N. Konstantinov, A. A. Harris, M. F. Hartshorne, and A. H. Tzamaloukas, “Symptomatic anti-neutrophil cytoplasmic antibody-positive disease complicating subacute bacterial endocarditis: to treat or not to treat?” Case Reports in Nephrology and Urology, vol. 2, pp. 25–32, 2012.
[108]
R. Angangco, S. Thiru, and D. B. G. Oliveira, “Pauci-immune glomerulonephritis associated with bacterial infection,” Nephrology Dialysis Transplantation, vol. 8, no. 8, pp. 754–756, 1993.
[109]
W. Hanf, J. E. Serre, J. H. Salmon et al., “Glomerulonephrite rapidement progressive a ANCA revelant une endocardite infectieuse subaigue (Rapidly progressive ANCA positive glomerulonephritis as the presenting feature of infectious endocarditis),” La Revue de Médecine Interne, vol. 32, pp. e116–e118, 2011.
[110]
B. Chan, V. d'Intini, and J. Savige, “Anti-neutrophil cytoplasmic antibody (ANCA)-associated microscopic polyangiitis following a suppurative wound infection,” Nephrology Dialysis Transplantation, vol. 21, no. 10, pp. 2993–2994, 2006.
[111]
M. Uh, I. A. McCormick, and J. T. Kelsall, “Positive cytoplasmic antineutrophil cytoplasmic antigen with PR3 specificity glomerulonephritis in a patient with subacute bacterial endocarditis,” Journal of Rheumatology, vol. 38, no. 7, pp. 1527–1528, 2011.
[112]
J. F. Viallard, S. Bonnet, L. Couzi et al., “Glomerulonephritis caused by Actinobacillus actinomycetemcomitans mimicking c-ANCA-positive vasculitis,” Nephrology Dialysis Transplantation, vol. 17, no. 4, pp. 663–665, 2002.
[113]
H. Sugiyama, M. Sahara, Y. Imai et al., “Infective endocarditis by Bartonella quintana masquerading as antineutrophil cytoplasmic antibody-associated small vessel vasculitis,” Cardiology, vol. 114, no. 3, pp. 208–211, 2009.
[114]
S. H. Forbes, S. C. Robert, J. E. Martin, and R. Rajakariar, “Acute kidney injury with hematuria, a positive ANCA test, and low levels of complement,” American Journal of Kidney Diseases, vol. 59, pp. 26–31, 2012.
[115]
A. Y. Elzouki, M. Akthar, and K. Mirza, “Brucella endocarditis associated with glomerulonephritis and renal vasculitis,” Pediatric Nephrology, vol. 10, no. 6, pp. 748–751, 1996.
[116]
H. Bonarek, F. Bonnet, C. Delclaux, C. Deminière, V. De Précigout, and M. Aparicio, “Reversal of c-ANCA positive mesangiocapillary glomerulonephritis after removal of an infected cysto-atrial shunt,” Nephrology Dialysis Transplantation, vol. 14, no. 7, pp. 1771–1773, 1999.
[117]
Y. Iwata, S. Ohta, K. Kawai et al., “Shunt nephritis with positive titers for ANCA specific for proteinase 3,” American Journal of Kidney Diseases, vol. 43, no. 5, pp. e11–e16, 2004.
[118]
T. Nagashima, D. Hirata, H. Yamamoto, H. Okazaki, and S. Minota, “Antineutrophil cytoplasmic autoantibody specific for proteinase 3 in a patient with shunt nephritis induced by Gemella morbillorum,” American Journal of Kidney Diseases, vol. 37, no. 5, article E38, 2001.
[119]
H. Takato, M. Yasui, Y. Waseda, N. Sakai, T. Wada, and M. Fujimura, “A case of microscopic polyangiitis following mycoplasma infection in a patient with MPO-ANCA positive pulmonary fibrosis,” Allergology International, vol. 60, no. 1, pp. 93–96, 2011.
[120]
P. Lamprecht, W. H. Schmitt, and W. L. Gross, “Mixed cryoglobulinaemia, glomerulonephritis, and ANCA: essential cryoglobulinaemic vasculitis or ANCA-associated vasculitis?” Nephrology Dialysis Transplantation, vol. 13, no. 1, pp. 213–221, 1998.
[121]
E. J. B. Monteiro, D. Caron, C. A. Balda, M. Franco, A. B. Pereira, and G. M. Kirsztajn, “Anti-glomerular basement membrane glomerulonephritis in an HIV positive patient: case report,” Brazilian Journal of Infectious Diseases, vol. 10, no. 1, pp. 55–58, 2006.
[122]
J. H. Song, K. J. Lee, S. W. Lee, J. Y. Han, and M. J. Kim, “Fatal pulmonary-renal syndrome manifested with immune complex crescentic glomerulonephritis in a patient with MPO-ANCA seropositivity,” Yonsei Medical Journal, vol. 42, no. 4, pp. 425–430, 2001.
[123]
T. Messiaen, C. Lefebvre, F. Zech, J. P. Cosyns, and M. Jadoul, “ANCA-positive rapidly progressive glomerulonephritis: there may be more to the diagnosis than you think!,” Nephrology Dialysis Transplantation, vol. 12, no. 4, pp. 839–841, 1997.
[124]
J. F. Subra, C. Michelet, J. Laporte et al., “The presence of cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA) in the course of subacute bacterial endocarditis with glomerular involvement, coincidence or association?” Clinical Nephrology, vol. 49, no. 1, pp. 15–18, 1998.
[125]
T. Haseyama, H. Imai, A. Komatsuda et al., “Proteinase-3-antineutrophil cytoplasmic antibody (PR3-ANCA) positive crescentic glomerulonephritis in a patient with Down's syndrome and infectious endocarditis,” Nephrology Dialysis Transplantation, vol. 13, no. 8, pp. 2142–2146, 1998.
[126]
K. Osafune, H. Takeoka, H. Kanamori et al., “Crescentic glomerulonephritis associated with infective endocarditis: renal recovery after immediate surgical intervention,” Clinical and Experimental Nephrology, vol. 4, no. 4, pp. 329–334, 2000.
[127]
K. Y. Wang, S. Shimajirt, T. Yoshida, S. Yamada, and Y. Sasagurt, “An autopsy case of microscopic polyangiitis associated with bacterial endocarditis,” Journal of University of Occupational and Environmental Health, vol. 32, no. 3, pp. 273–279, 2010.
[128]
D. Sitara and B. I. Hoffbrand, “Chronic bronchial suppuration and antineutrophil cytoplasmic antibody (ANCA) positive systemic vasculitis,” Postgraduate Medical Journal, vol. 66, no. 778, pp. 669–671, 1990.
[129]
M. Haas and J. A. Eustace, “Immune complex deposits in ANCA-associated crescentic glomerulonephritis: a study of 126 cases,” Kidney International, vol. 65, no. 6, pp. 2145–2152, 2004.
[130]
F. Yu, M. Chen, S. X. Wang, W. Z. Zou, M. H. Zhao, and H. Y. Wang, “Clinical and pathological characteristics and outcomes of Chinese patients with primary anti-neutrophil cytoplasmic antibodies-associated systemic vasculitis with immune complex deposition in kidney,” Nephrology, vol. 12, no. 1, pp. 74–80, 2007.
[131]
L. Cavagna, R. Caporali, C. Esposito, C. Augetti, O. Epis, and C. Montecucco, “Clinical features of ANCA-positive systemic lupus erythematosus: report of two cases,” Scandinavian Journal of Rheumatology, vol. 36, no. 1, pp. 74–76, 2007.
[132]
Y. Hirai, M. Iyoda, T. Shibata et al., “Lupus nephritis associated with positive MPO-ANCA in a patient with underlying autoimmune hemolytic anemia,” Clinical and Experimental Nephrology, vol. 12, no. 5, pp. 393–397, 2008.
[133]
S. H. Nasr, V. D. D’Agati, H.-R. Park et al., “Necrotizing and crescentic lupus nephritis with antineutrophil cytoplasmic seropositivivity,” Clinical Journal of the American Society of Nephrology, vol. 3, pp. 682–690, 2008.
[134]
S. Mezzano, G. Valderrama, F. Olavarria et al., “Antineutrophil-cytoplasmic-autoantibodies in poststreptococcal nephritis,” Advances in Experimental Medicine and Biology, vol. 336, pp. 449–453, 1993.
[135]
A. Waters, V. Langlois, P. Thorner, and D. Geary, “Atypical p-ANCA is not a poor prognostic marker in postinfectious glomerulonephritis,” Pediatric Nephrology, vol. 22, no. 9, pp. 1383–1386, 2007.
[136]
L. G. Ardiles, G. Valderrama, P. Moya, and S. A. Mezzano, “Incidence and studies on antigenic specificities of antineutrophil-cytoplasmic autoantibodies (ANCA) in poststreptococcal glomerulonephritis,” Clinical Nephrology, vol. 47, no. 1, pp. 1–5, 1997.
[137]
I. Neumann, H. Regele, R. Kain, R. Birck, and F. T. Meisl, “Glomerular immune deposits are associated with increased proteinuria in patients with ANCA-associated crescentic nephritis,” Nephrology Dialysis Transplantation, vol. 18, no. 3, pp. 524–531, 2003.
[138]
S. H. Nasr, S. M. Said, A. M. Valeri et al., “Membranous glomerulonephritis with ANCA-associated necrotizing and crescentic glomerulonephritis,” Clinical Journal of the American Society of Nephrology, vol. 4, no. 2, pp. 299–308, 2009.
[139]
E. Wechsler, T. Yang, S. C. Jordan, A. Vo, and C. C. Nast, “Anti-glomerular basement membrane disease in an HIV-infected patient,” Nature Clinical Practice Nephrology, vol. 4, no. 3, pp. 167–171, 2008.
[140]
P. Singh, M. Barry, and A. Tzamaloukas, “Goodpasture’s disease complicating human immunodeficiency virus infection,” Clinical Nephrology, vol. 76, pp. 74–77, 2011.
[141]
A. Davenport, J. Goodfellow, S. Goel, A. G. Maciver, and P. Walker, “Aortic valve disease in patients with Wegener's granulomatosis,” American Journal of Kidney Diseases, vol. 24, no. 2, pp. 205–208, 1994.
[142]
A. D. Fox and S. E. Robbins, “Aortic valvulitis complicating Wegener's granulomatosis,” Thorax, vol. 49, no. 11, pp. 1176–1177, 1994.
[143]
S. C. D. Grant, R. D. Levy, M. C. Venning, C. Ward, and N. H. Brooks, “Wegener's granulomatosis and the heart,” British Heart Journal, vol. 71, no. 1, pp. 82–86, 1994.
[144]
N. E. R. Goodfield, S. Bhandari, W. D. Plant, A. Morley-Davies, and G. R. Sutherland, “Cardiac involvement in Wegener's granulomatosis,” British Heart Journal, vol. 73, no. 2, pp. 110–115, 1995.
[145]
R. D. Leff, “Acute aortic insufficiency associated with Wegener granulomatosis,” Mayo Clinic Proceedings, vol. 74, no. 9, pp. 897–899, 1999.
[146]
P. Bruno, C. Le Hello, M. Massetti et al., “Necrotizing granulomata of the aortic valve in Wegener's disease,” Journal of Heart Valve Disease, vol. 9, no. 5, pp. 633–635, 2000.
[147]
J. M. Mishell, “Cases from the Osler Medical Service at Johns Hopkins University,” American Journal of Medicine, vol. 113, no. 7, pp. 607–609, 2002.
[148]
M. Calachanis, P. Ferrero, F. Orzan, F. Marchisio, and G. Trevi, “Vasculitis mimicking bacterial endocarditis,” Italian Heart Journal, vol. 4, no. 11, pp. 816–818, 2003.
[149]
C. St？llberger, J. Finsterer, G. J. Zlabinger et al., “Antineutrophil cytoplasmic autoantibody-negative antiproteinase 3 syndrome presenting as vasculitis, endocarditis, polyneuropathy and Dupuytren's contracture,” Journal of Heart Valve Disease, vol. 12, no. 4, pp. 530–534, 2003.
[150]
S. Ramakrishnan, R. Narang, G. C. Khilnani et al., “Wegener's granulomatosis mimicking prosthetic valve endocarditis,” Cardiology, vol. 102, no. 1, pp. 35–36, 2004.
[151]
J. A. Savige, L. Chang, S. Horn, and S. M. Crowe, “Anti-nuclear, anti-neutrophil cytoplasmic and anti-glomerular basement membrane antibodies in HIV-infected individuals,” Autoimmunity, vol. 18, no. 3, pp. 205–211, 1994.
[152]
G. T. Hernandez, J. M. Critchfield, and R. A. Rodriguez, “Interpretation of serologic tests in an HIV-infected patient with kidney disease,” Nature Clinical Practice Nephrology, vol. 2, no. 12, pp. 708–712, 2006.
[153]
L. A. Szczech, A. Anderson, C. Ramers et al., “The uncertain significance of anti-glomerular basement membrane antibody among HIV-infected persons with kidney disease,” American Journal of Kidney Diseases, vol. 48, no. 4, pp. e55–e59, 2006.
[154]
M. P. Muthiah, “New lung lesion in immunocompromised host—correct diagnosis despite a false positive ANCA,” Southern Medical Journal, vol. 99, no. 7, pp. 701–702, 2006.
[155]
M. Koselj-Kajtna, M. Koselj, T. Rott, A. Kandus, and A. Bren, “Infectious complications of immunosuppressive treatment for anti-neutrophil cytoplasm antibody-related vasculitis,” Transplantation Proceedings, vol. 34, no. 7, pp. 3001–3002, 2002.
[156]
C. Charlier, C. Henegar, O. Launay et al., “Risk factors for major infections in Wegener granulomatosis: analysis of 113 patients,” Annals of the Rheumatic Diseases, vol. 68, no. 5, pp. 658–663, 2009.
[157]
J. G. McGregor, S. L. Hogan, Y. Hu, C. E. Jennette, R. J. Falk, and P. H. Nachman, “Glucocorticoids and relapse and infection rates in anti-neutrophil cytoplasmic antibody disease,” Clinical Journal of the American Society of Nephrology, vol. 7, pp. 240–247, 2012.
[158]
Y. Nagaba, Y. Hiki, T. Aoyama et al., “Effective antibiotic treatment of methicillin-resistant Staphylococcus aureus-associated glomerulonephritis,” Nephron, vol. 92, no. 2, pp. 297–303, 2002.
[159]
D. Jovanovi？, Z. Kovacevi？, V. Rabrenovi？, and V. Skatari？, “Acute post-streptococcal glomerulonephritis in adults—corticosteroid therapy, yes or no?” Vojnosanitetski Pregled, vol. 58, no. 2, pp. 161–166, 2001.
[160]
V. Le Moing, F. Lacassin, M. Delahousse et al., “Use of corticosteroids in glomerulonephritis related to infective endocarditis: three cases and review,” Clinical Infectious Diseases, vol. 28, no. 5, pp. 1057–1061, 1999.
[161]
D. Koya, K. Shibuya, R. Kikkawa, and M. Haneda, “Successful recovery of infective endocarditis-induced rapidly progressive glomerulonephritis by steroid therapy combined with antibiotics: a case report,” BMC Nephrology, vol. 5, article 18, 2004.
[162]
A. S. Wiik, “Autoantibodies in ANCA-associated vasculitis,” Rheumatic Disease Clinics, vol. 36, pp. 479–489, 2010.
[163]
C. G. M. Kallenberg, “Pathogenesis of ANCA-associated vasculitides,” Annals of the Rheumatic Diseases, vol. 70, no. 1, supplement, pp. i59–i63, 2011.
[164]
N. Lepse, W. H. Abdulahad, C. G. M. Kallenberg, and P. Heeringa, “Immune regulatory mechanisms in ANCA-associated vasculitides,” Autoimmunity Reviews, vol. 11, pp. 77–83, 2011.
[165]
M. M. van Timmeren and P. Heeringa, “Pathogenesis of ANCA-associated vasculitis: recent insights from animal models,” Current Opinion in Rheumatology, vol. 24, pp. 8–14, 2012.
[166]
M. A. Little, B. Al-Ani, S. Ren et al., “Anti-proteinase 3 anti-neutrophil cytoplasm autoantibodies recapitulate systemic vasculitis in mice with a humanized immune system,” PLoS One, vol. 7, Article ID e28626, 2012.
[167]
Y. Hong, D. Eleftheriou, A. A. Hussain et al., “Anti-neutrophil cytoplasmic antibodies stimulate release on neutrophil microparticles,” Journal of the American Society of Nephrology, vol. 23, pp. 49–62, 2012.
[168]
C. A. Stegeman, J. W. C. Tervaert, W. J. Sluiter, W. L. Manson, P. E. De Jong, and C. G. M. Kallenberg, “Association of chronic nasal carriage of Staphylococcus aureus and higher relapse rates in Wegener granulomatosis,” Annals of Internal Medicine, vol. 120, no. 1, pp. 12–17, 1994.
[169]
M. Laudien, S. D. Gadola, R. Podschun et al., “Nasal carriage of Staphylococcus aureus and endonasal activity in Wegener’s granulomatosis as compared to rheumatoid arthritis and chronic rhinosinusitis with nasal polyps,” Clinical and Experimental Rheumatology, vol. 28, supplement 57, pp. 51–55, 2010.
[170]
E. R. Popa, C. A. Stegeman, C. G. M. Kallenberg, and J. W. C. Tervaert, “Staphylococcus aureus and Wegener's granulomotosis,” Arthritis Research, vol. 4, no. 2, pp. 77–79, 2002.
[171]
M. Chen and C. G. M. Kallenberg, “ANCA-associated vasculitides-advances in pathogenesis and treatment,” Nature Reviews Rheumatology, vol. 6, no. 11, pp. 653–664, 2010.
[172]
J. Savige, L. Nassis, T. Cooper, B. Paspaliaris, P. Martinello, and D. MacGregor, “Antineutrophil cytoplasmic antibody (ANCA)-associated systemic vasculitis after immunization with bacterial proteins,” Clinical and Experimental Rheumatology, vol. 20, pp. 783–789, 2002.
[173]
H. Tadema, W. H. Abdulahad, N. Lepse, C. A. Stegeman, C. G. M. Kallenberg, and P. Heeringa, “Bacterial DNA motifs trigger ANCA production in ANCA-associated vasculitis in remission,” Rheumatology, vol. 50, no. 4, pp. 689–696, 2011.
[174]
R. A. DeRemee, T. J. McDonald, and L. H. Weiland, “Wegener's granulomatosis: observations on treatment with antimicrobial agents,” Mayo Clinic Proceedings, vol. 60, no. 1, pp. 27–32, 1985.
[175]
B. C. West, J. R. Todd, and J. W. King, “Wegener granulomatosis and trimethoprim-sulfamethoxazole: complete remission after a twenty-year course,” Annals of Internal Medicine, vol. 106, no. 6, pp. 840–842, 1987.
[176]
H. L. Israel, “Sulfamethoxazole-trimethoprim therapy for Wegener's granulomatosis,” Archives of Internal Medicine, vol. 148, no. 10, pp. 2293–2295, 1988.
[177]
C. A. Stegeman, J. W. C. Tervaert, P. E. De Jong, and C. G. M. Kallenberg, “Trimethoprim-sulfamethoxazole (Co-trimoxazole) for the prevention of relapses of Wegener's granulomatosis,” New England Journal of Medicine, vol. 335, no. 1, pp. 16–20, 1996.
[178]
C. G. M. Kallenberg, “What is the evidence for prophylactic antibiotic treatment in patients with systemic vasculitides?” Current Opinion in Rheumatology, vol. 23, no. 3, pp. 311–316, 2011.
[179]
E. R. Popa, C. A. Stegeman, N. A. Bos, C. G. M. Kallenberg, and J. W. Cohen Tervaert, “Staphylococcal superantigens and T cell expansions in Wegener's granulomatosis,” Clinical and Experimental Immunology, vol. 132, no. 3, pp. 496–504, 2003.
[180]
E. R. Popa, C. A. Stegeman, W. H. Abdulahad et al., “Staphylococcal toxic-shock-syndrome-toxin-1 as a risk factor for disease relapse in Wegener's granulomatosis,” Rheumatology, vol. 46, no. 6, pp. 1029–1033, 2007.
[181]
W. F. Pendergraft, G. A. Preston, R. R. Shah et al., “Autoimmunity is triggered by cPR-3(105–201), a protein complementary to human autoantigen proteinase-3,” Nature Medicine, vol. 10, no. 1, pp. 72–79, 2004.
[182]
P. Hewins, F. Belmonte, J. Charles Jennette, R. J. Falk, and G. A. Preston, “Longitudinal studies of patients with ANCA vasculitis demonstrate concurrent reactivity to complementary PR3 protein segments cPR3m and cPR3C and with no reactivity to cPR3N,” Autoimmunity, vol. 44, no. 2, pp. 98–106, 2011.
[183]
J. C. Jennette, R. J. Falk, and A. H. Gasim, “Pathogenesis of antineutrophil cytoplasmic autoantibody vasculitis,” Current Opinion in Nephrology and Hypertension, vol. 20, no. 3, pp. 263–270, 2011.
[184]
M. H. Zhao, S. J. Jones, and C. M. Lockwood, “Bactericidal/permeability-increasing protein (BPI) is an important antigen for anti-neutrophil cytoplasmic autoantibodies (ANCA) in vasculitis,” Clinical and Experimental Immunology, vol. 99, no. 1, pp. 49–56, 1995.
[185]
M. H. Zhao and C. M. Lockwood, “Azurocidin is a novel antigen for anti-neutrophil cytoplasmic autoantibodies (ANCA) in systemic vasculitis,” Clinical and Experimental Immunology, vol. 103, no. 3, pp. 397–402, 1996.
[186]
M. P. Stoffel, E. Csernok, C. Herzberg, T. Johnston, S. F. Carroll, and W. L. Gross, “Anti-neutrophil cytoplasmic antibodies (ANCA) directed against bactericidal/permeability increasing protein (BPI): a new seromarker for inflammatory bowel disease and associated disorders,” Clinical and Experimental Immunology, vol. 104, no. 1, pp. 54–59, 1996.
[187]
H. Schultz, “From infection to autoimmunity: a new model for induction of ANCA against the bactericidal/permeability increasing protein (BPI),” Autoimmunity Reviews, vol. 6, no. 4, pp. 223–227, 2007.
[188]
J. J. Yang, R. Tuttle, R. J. Falk, and J. C. Jennette, “Frequency of anti-bactericidal/permeability-increasing protein (BPI) and anti-azurocidin in patients with renal disease,” Clinical and Experimental Immunology, vol. 105, no. 1, pp. 125–131, 1996.
[189]
R. Kain, M. Exner, R. Brandes et al., “Molecular mimicry in pauci-immune focal necrotizing glomerulonephritis,” Nature Medicine, vol. 14, no. 10, pp. 1088–1096, 2008.
[190]
X. Bosch and E. Mirapeix, “LAMP-2 illuminates pathogenesis of ANCA glomerulonephritis,” Nature Reviews Nephrology, vol. 5, no. 5, pp. 247–249, 2009.
[191]
A. D. Salama and C. D. Pusey, “Shining a LAMP on pauci-immune focal segmental glomerulonephritis,” Kidney International, vol. 76, no. 1, pp. 15–17, 2009.
[192]
A. J. Roth, M. C. Brown, E. N. Smith, et al., “Anti-LAMP-2 antibodies are not prevalent in patients with antineutrophil cytoplasmic antibody glomerulonephritis,” Journal of the American Society of Nephrology, vol. 23, pp. 545–555, 2012.
[193]
S. M. Flint and C. O. Savage, “Anti-LAMP-2 autoantibodies in ANCA-associated pauci-immune glomerulonephritis,” Journal of the American Society of Nephrology, vol. 23, pp. 378–380, 2012.
[194]
V. Brinkmann, U. Reichard, C. Goosmann et al., “Neutrophil extracellular traps kill bacteria,” Science, vol. 303, no. 5663, pp. 1532–1535, 2004.
[195]
T. A. Fuchs, U. Abed, C. Goosmann et al., “Novel cell death program leads to neutrophil extracellular traps,” Journal of Cell Biology, vol. 176, no. 2, pp. 231–241, 2007.
[196]
K. Kessenbrock, M. Krumbholz, U. Sch？nermarck et al., “Netting neutrophils in autoimmune small-vessel vasculitis,” Nature Medicine, vol. 15, no. 6, pp. 623–625, 2009.
[197]
X. Bosch, “LAMPs and NETs in the pathogenesis of ANCA vasculitis,” Journal of the American Society of Nephrology, vol. 20, no. 8, pp. 1654–1656, 2009.
[198]
T. Kawai and S. Akira, “The role of pattern-recognition receptors in innate immunity: update on toll-like receptors,” Nature Immunology, vol. 11, no. 5, pp. 373–384, 2010.
[199]
H. Tadema, W. H. Abdulahad, N. Lepse, C. A. Stegeman, C. G. M. Kallenberg, and P. Heeringa, “Bacterial DNA motifs trigger ANCA production in ANCA-associated vasculitis in remission,” Rheumatology, vol. 50, no. 4, pp. 689–696, 2011.
[200]
H. Tadema, W. H. Abdulahad, C. A. Stegeman, C. G. M. Kallenberg, and P. Heeringa, “Increased expression of Toll-like receptors by monocytes and natural killer cells in ANCA-associated vasculitis,” PLoS One, vol. 6, no. 9, Article ID e24315, 2011.
[201]
H. Morris, M. D. Morgan, A. M. Wood, et al., “ANCA-associated vasculitis is linked to carriage of the Z allele of α1 antitrypsin and its polymers,” Annals of the Rheumatic Diseases, vol. 70, pp. 1851–1856, 2011.
[202]
P. A. Lyons, T. F. Rayner, S. Trivedi, et al., “Genetically distinct subsets within ANCA-associated vasculitis,” New England Journal of Medicine, vol. 367, pp. 214–223, 2012.
[203]
D. Martorana, F. Maritati, and G. Malebra, “PTRN22 R620W polymorphism in the ANCA-associated vasculitides,” Rheumatology, vol. 51, pp. 805–812, 2012.
[204]
L. C. Willcocks, P. A. Lyons, A. J. Rees, and K. G. C. Smith, “The contribution of genetic variation and infection to the pathogenesis of ANCA-associated systemic vasculitis,” Arthritis Research and Therapy, vol. 12, no. 1, article 202, 2010.
