Drug-induced glomerular disease: immune-mediated injury - PubMed (original) (raw)

Review

. 2015 Jul 7;10(7):1300-10.

doi: 10.2215/CJN.01910215. Epub 2015 Jun 19.

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Review

Drug-induced glomerular disease: immune-mediated injury

Jonathan J Hogan et al. Clin J Am Soc Nephrol. 2015.

Abstract

Drug-induced autoimmune disease was initially described decades ago, with reports of vasculitis and a lupus-like syndrome in patients taking hydralazine, procainamide, and sulfadiazine. Over the years, multiple other agents have been linked to immune-mediated glomerular disease, often with associated autoantibody formation. Certain clinical and laboratory features may distinguish these entities from their idiopathic counterparts, and making this distinction is important in the diagnosis and management of these patients. Here, drug-induced, ANCA-associated vasculitis, drug-induced lupus, and drug-associated membranous nephropathy are reviewed.

Keywords: ANCA; GN; SLE; drug nephrotoxicity; membranous nephropathy.

Copyright © 2015 by the American Society of Nephrology.

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Figures

Figure 1.

Figure 1.

A glomerulus from a patient who used cocaine that contained levamisole and presented with rapidly progressive GN and high-titer anti-myeloperoxidase ANCA. The glomerulus exhibits fibrinoid necrosis, multifocal rupture of the glomerular basement membrane, and an overlying, circumferential cellular crescent. Jones methenamine silver, ×400.

Figure 2.

Figure 2.

Digital cutaneous vasculitis of a patient with levamisole-associated, ANCA-associated vasculitis. Reprinted from Joan Von Feldt and Robert Michelleti, with permission.

Figure 3.

Figure 3.

A glomerulus from a patient who developed nephrotic syndrome while receiving a nonsteroidal anti-inflammatory drug for arthritis. The glomerulus exhibits global thickening of the glomerular basement with spike formation, which is characteristic of stage 2 membranous changes. Jones methenamine silver, ×400.

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