Alemtuzumab-induced antineutrophil cytoplasmic antibody-associated nephritis in a patient with multiple sclerosis
Furkan Sarıdaş1
, Saide Elif Güllülü Boz2, Belkıs Nihan Coşkun3, Emine Rabia Koç1, Abdulmecit Yıldız2, Berna Aytaç Vuruşkan4, Ömer Faruk Turan1
1Department of Neurology, Bursa Uludağ University Faculty of Medicine, Bursa, Türkiye
2Department of Nephrology, Bursa Uludağ University Faculty of Medicine, Bursa, Türkiye
3Department of Rheumatology, Bursa Uludağ University Faculty of Medicine, Bursa, Türkiye
4Department of Pathology, Bursa Uludağ University Faculty of Medicine, Bursa, Türkiye
Keywords: Alemtuzumab, ANCA-associated vasculitis, multiple sclerosis, renal failure.
Abstract
Alemtuzumab (ATZ), a potent disease-modifying drug used to treat relapsing-remitting multiple sclerosis, is a humanized anti-CD52 monoclonal antibody that causes profound depletion of B and T lymphocytes. Despite its potent immunosuppressive effect, paradoxically secondary autoimmune disorders, notably thyroid disease, were reported following ATZ treatment. There were few reports of ATZ-associated renal disease in the form of membranous glomerulonephritis and anti-glomerular basement membrane disease. In this article, we reported a 45-year-old female patient with relapsing-remitting multiple sclerosis with ANCA (antineutrophil cytoplasmic antibody)-associated vasculitis resulting in rapidly progressive glomerulonephritis limited to the kidney after ATZ treatment.
Cite this article as: Sarıdaş F, Güllülü Boz SE, Coşkun BN, Koç ER, Yıldız A, Aytaç Vuruşkan B, et al. Alemtuzumab-induced antineutrophil cytoplasmic antibody-associated nephritis in a patient with multiple sclerosis. Turk J Neurol 2025;31(2):229-231. doi: 10.55697/tnd.2024.238.
The data that support the findings of this study are available from the corresponding author upon reasonable request.
Idea/concept: F.S., S.E.G., Ö.F.T.; Design, writing the article: F.S., S.E.G.; Control/ supervision: B.N.C., A.Y., Ö.F.T.; Data collection and/or processing: F.S., S.E.G., B.N.C., B.A.V.; Analysis and/or interpretation: B.N.C., A.Y., B.A.V., Ö.F.T.; Literature review: F.S., S.E.G., B.N.C.; Critical review: B.N.C., A.Y., Ö.F.T.; References and fundings: F.S., B.N.C., E.R.K.; Materials: B.N.C., E.R.K., A.Y., B.A.V., Ö.F.T.
The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.
The authors received no financial support for the research and/or authorship of this article.