%0 Journal Article
%T Glomerular Disease in Patients with Infectious Processes Developing Antineutrophil Cytoplasmic Antibodies
%A Konstantin N. Konstantinov
%A Suzanne N. Emil
%A Marc Barry
%A Susan Kellie
%A Antonios H. Tzamaloukas
%J ISRN Nephrology
%D 2013
%R 10.5402/2013/324315
%X 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
%U http://www.hindawi.com/journals/isrn.nephrology/2013/324315/