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      Methimazole-Induced Pauci-Immune Glomerulonephritis and Anti-Phospholipid Syndrome: An Important Association to Be Aware of

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          Abstract

          While methimazole (MMI) is the first line treatment for hyperthyroidism, this medication is not devoid of adverse effects. In this article, we present a 70-year-old male who admitted the hospital with right lower extremity pain and rash. The patient was recently treated with MMI for hyperthyroidism. Imaging studies revealed bilateral renal and splenic infarcts along with thrombosis of popliteal artery. Laboratory data revealed hematuria and proteinuria with positive (MPO), anti-proteinase-3 (PR3) and anti-cardiolipin IgG antibodies. Renal biopsy revealed pauci-immune glomerulonephritis and features with anti-phospholipid antibody syndrome (APS). MMI was discontinued and the patient was treated successfully with steroid therapy and anti-coagulation with resolution of proteinuria, hematuria and normalization of laboratory parameters. While MMI-induced pauci-immune glomerulonephritis has been previously reported, its association with APS has never been described before. Our case demonstrates that this rare diagnosis can be treated by early withdrawal of MMI and initiation of steroids along with anticoagulation.

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          Most cited references25

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          Rapidly progressive crescentic glomerulonephritis: Early treatment is a must.

          The term crescentic glomerulonephritis (GN) refers to a pathologic condition characterized by extracapillary proliferation in >50% of glomeruli. Clinically crescentic GN is characterized by a nephritic syndrome rapidly progressing to end stage renal disease (ESRD). Three types of crescentic GN have been identified. Type 1 includes cases of Goodpasture syndrome characterized by linear deposits of antibodies along the glomerular basement membrane (GBM) at immunofluorescence. Type 2 is a heterogeneous group of primary or secondary glomerular diseases complicated by crescentic GN. In this category there are granular deposits of immunoglobulins and complement fractions on the glomerular tuft. Type 3 includes cases of ANCA-associated small-vessel vasculitis. Immunofluorescence is negative or may show only faint deposits of immunoglobulins. The etiology and the initial pathogenetic factors are different in the three types, but the final mechanisms leading to crescent formation and the renal symptoms and signs are similar. The prognosis depends on the timeline of diagnosis and treatment. Although some patients requiring dialysis may recover a good renal function, usually the higher the serum creatinine at presentation the worse the outcome. When treatment is initiated early, most patients obtain a complete or partial remission. High-dose corticosteroids and cyclophosphamide represent the standard therapy for crescentic GN. The addition of plasma exchange may also be helpful, particularly in patients with massive alveolar hemorrhage. Anti-B monoclonal antibodies have also been used in some patients with crescentic GN, but their role in this particular area is still poorly established.
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            Rapidly progressive glomerulonephritis: classification, pathogenetic mechanisms, and therapy.

            W Couser (1988)
            Immunopathologic studies over the past two decades have demonstrated that rapidly progressive glomerulonephritis (RPGN) can result from glomerular deposition of anti-GBM antibody, immune complexes, or from some as yet undefined mechanism that does not involve glomerular antibody deposition. The latter process may be cell mediated and resembles a small vessel vasculitis. Most cases of idiopathic RPGN are not accompanied by pathogenic glomerular immunoglobulin deposition. Recent experimental studies of immune mechanisms of glomerular injury have identified several new processes that can induce damage to the capillary wall sufficient to result in crescentic glomerulonephritis (GN). These include direct effects of anti-GBM antibody alone and of the complement C5b-9 (membrane attack) complex, nephritogenic effects of inflammatory effector cells that involve reactive oxygen species and glomerular halogenation, and injury mediated by sensitized lymphocytes independently of antibody deposition. Macrophages have been shown to participate in both intracapillary and extracapillary fibrin deposition and crescent formation as well as to mediate capillary wall damage. The role of resident glomerular cells and cell-cell interactions in glomerulonephritis is still under active investigation. Despite these several advances in understanding immune injury to the glomerulus, therapy for RPGN remains largely empiric. Although the prognosis in RPGN has clearly improved over time, no form of disease-specific therapy has been clearly shown yet to be beneficial in a controlled study. Interpretation of the existing literature on therapy is complicated by the availability of only historical rather than concurrent controls, lack of attention to several variables known to affect disease outcome, and uncertainty regarding bias in favor of reporting positive results. Available data suggests that optimal outcomes may be achieved in anti-GBM nephritis by treatment with steroids, immunosuppression and plasma exchange, particularly when therapy is directed at patients with mild but rapidly progressive disease before oliguria or severe azotemia develop. Pulse steroids are probably the most cost-effective therapy for the idiopathic form of RPGN, but treatment with cytotoxic agents should be considered if clinical or histologic evidence of vasculitis is present.
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              Review article: Drug-induced anti-neutrophil cytoplasmic antibody-associated vasculitis.

              A recent development in the field of vasculitis is the increasing recognition that certain medications such as propylthiouracil can induce anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV). This review focuses on the data on causal drugs, possible pathogenesis, clinical description, diagnosis, treatment and prognosis of patients with drug-induced AAV. The pathogenesis of drug-induced AAV might be multifactorial. The clinical manifestations are similar to those of primary AAV, but ANCA with multi-antigenicity may help to differentiate it from primary AAV. The diagnosis of drug-induced AAV is based on the temporal relationship between clinically evident vasculitis and administration of the offending drugs, and excluding medical conditions that mimic vasculitis and other definable types of vasculitis. After the diagnosis of drug-induced AAV was made, the offending drugs should be withdrawn immediately, and appropriate immunosuppressive therapy should be administered only for patients with vital organ involvement. The duration of immunosuppressive therapy should be much shorter than that in primary AAV and long-term maintenance therapy might not be necessary. The prognosis of patients with drug-induced AAV is good as long as the offending drug is discontinued in time.
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                Author and article information

                Journal
                J Clin Med Res
                J Clin Med Res
                Elmer Press
                Journal of Clinical Medicine Research
                Elmer Press
                1918-3003
                1918-3011
                October 2018
                10 September 2018
                : 10
                : 10
                : 786-790
                Affiliations
                [a ]Department of Medicine, Jersey Shore University Medical Center, Hackensack Meridian Health, Neptune, NJ 07753, USA
                [b ]Department of Pathology, Jersey Shore University Medical Center, Hackensack Meridian Health, Neptune, NJ 07753, USA
                [c ]Department of Pathology, Columbia University Medical Center, NY Presbyterian/Columbia, New York, NY 10032, USA
                Author notes
                [d ]Corresponding Author: Arif Asif, Department of Medicine, Jersey Shore University Medical Center, Hackensack Meridian School of Medicine at Seton Hall, 1945 Route 33, Neptune, NJ, USA. Email: arif.asif@ 123456hackensackmeridian.org
                Article
                10.14740/jocmr3530w
                6135002
                c044e253-ca8f-41fa-9d99-14a4f11d31d0
                Copyright 2018, Qaisar et al.

                This article is distributed under the terms of the Creative Commons Attribution Non-Commercial 4.0 International License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 25 July 2018
                : 30 August 2018
                Categories
                Case Report

                Medicine
                methimazole,pauci-immune,crescentic glomerulonephritis,ana,glucocorticosteroids
                Medicine
                methimazole, pauci-immune, crescentic glomerulonephritis, ana, glucocorticosteroids

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