To describe a unique presentation of immune-mediated nephropathy and concurrent relapsing multiple sclerosis (RMS) exacerbation after induction with Alemtuzumab in a patient with highly active MS.

Alemtuzumab is a cytolytic CD52-binding monoclonal antibody approved as a disease-modifying treatment of RMS. While it has been associated with significant improvement in relapses and disability outcomes, Alemtuzumab also carries the risk of adverse events, specifically autoimmune reactions. The more commonly described renal immune response is anti-GBM nephrotic disease. This case details a unique nephrotic reaction six weeks after Alemtuzumab induction in the setting of an MS relapse.

A 28-year-old female with recent diagnosis of highly active MS with multifocal enhancing lesions throughout the central nervous system, and T1 hypointensities from initial presentation, was initiated on Alemtuzumab. Despite tolerating the infusion well, six weeks later she presented with rapid decline in mentation, worsening tremors and abdominal pain. Imaging revealed multiple new enhancing lesions indicating a relapse. Urinalysis was pertinent for a new diagnosis of hematuria, nephrotic grade proteinuria, and RBC casts. Anti-GBM antibodies were negative. Renal ultrasound revealed bilateral parenchymal disease and renal biopsy demonstrated glomerular mesangial IgA deposition suggestive of IgA nephropathy. She received treatment with high dose steroids to address the MS relapse as well as IgA nephropathy. At her 1-year follow up, the patient continues to improve neurologically and her renal parameters are stable, indicating no further progression of the IgA nephropathy.

IgA nephropathy after Alemtuzumab initiation has yet to be reported as an adverse event in literature to our knowledge, though the safety profile is still being determined in post-market surveillance. This case highlights a novel but treatable complication of Alemtuzumab and emphasizes the unpredictable timeline of such adverse events. Early diagnosis and initiation of steroids in similar clinical scenarios can prevent long-term decline in renal function.