Report of a patient with rheumatoid arthritis developing rapidly progressive glomerulonephritis associated with anti-glomerular basement membrane antibody and antineutrophil cytoplasmic antibody

Abstract

Rapidly progressive glomerulonephritis occurred in a 63-year-old woman with rheumatoid arthritis who had been treated with oral prednisolone for 5 years. Microscopic examination of the renal biopsy specimen showed marked obliteration of the tufts with noticeable cellular crescent formation in all glomeruli. Immunofluorescence staining of the biopsy specimen showed linear deposits of immunoglobulin G (IgG) diffused along the capillary walls. The serologic examination was positive for antiglomerular basement membrane antibody and perinuclear antineutrophil cytoplasmic antibody. Despite a tentative trial of plasma exchange and intensive combined therapy (intravenous administration of heparin and pulse therapy of methylprednisolone and cyclophosphamide), renal function progressively deteriorated and no recovery occurred.

Chronic Rheumatoid Arthritis Complicated by Myeloperoxidase Antineutrophil Cytoplasmic Antibody-Associated Nephritis

“…Thus, in patients like ours who develop cellular crescentic glomerulonephritis, the association between their pathology and MPO-ANCA is considered to be substantial. MPO-ANCA-associated nephritis has been suggested to be prone to serious complications such as pulmonary hemorrhage, and it could be concluded that such complications are related to these antibodies [9,10]. Therefore, we performed double-filtration plasmapheresis in the present patient with the aim of eliminating MPO-ANCA.…”

Crescentic glomerulonephritis with antimyeloperoxidase antibodies developing during the course of IgA nephropathy in a patient with rheumatoid arthritis

“…7 Recently, p-ANCA-positive crescentic glomerulonephritis has been documented sporadically in RA patients. 8,9 IgA nephropathy is the most common form of glomerulonephritis in the world, 10 and the occurrence of IgA nephropathy has been demonstrated in some patients with RA. 3 However, in such cases, it is difficult to be sure whether primary IgA nephropathy occurs during the course of RA, or secondary IgA nephropathy occurs as a form of RA nephropathy.…”