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Abstract: TH-PO577

Membranous Nephropathy Associated with Alemtuzumab

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis

Authors

  • Ravender, Raja, The University of New Mexico, Albuquerque, New Mexico, United States
  • Pal, Chaitanya A., The University of New Mexico, Albuquerque, New Mexico, United States
  • Kodavanti, Chandra Kumar Mallick, The University of New Mexico, Albuquerque, New Mexico, United States
  • Shaffi, Saeed Kamran, The University of New Mexico, Albuquerque, New Mexico, United States
  • Schmidt, Darren W., The University of New Mexico, Albuquerque, New Mexico, United States
  • Teixeira, J. Pedro, The University of New Mexico, Albuquerque, New Mexico, United States
  • Caza, Tiffany, Arkana Laboratories, Little Rock, Arkansas, United States
  • Garcia, Pablo, The University of New Mexico, Albuquerque, New Mexico, United States

Group or Team Name

  • UNMH/Arkana Team.
Introduction

Alemtuzumab is a humanized anti-CD52 monoclonal antibody approved for multiple sclerosis. We present a case of membranous nephropathy associated with alemtuzumab use.

Case Description

A 20-year-old woman with a seven-year history of multiple sclerosis was referred to nephrology due to new-onset nephrotic range proteinuria nine months after receiving her first cycle of alemtuzumab. She took no other medications. Vitals were stable with trace lower extremity edema. Spot urine protein- and albumin- to creatinine ratios were 4.63 g/g and 3481 mg/g, respectively. Serum creatinine was 0.4 mg/dL with serum albumin 2.1 g/dL. Hepatitis B and C, HIV, C3 and C4 complement, kappa/lambda ratio, anti-GBM antibody, rheumatoid factor, antinuclear antibody, antineutrophil cytoplasmic antibody, and anti-phospholipase A2 receptor (PLA2R) antibody were all negative. Renal biopsy revealed membranous nephropathy, with negative immunohistochemical stains for PLA2R, thrombospondin type-1 domain-containing 7A, exostosin 2, and neural epidermal growth factor-like 1. Alemtuzumab was held. Rituximab was initiated as it is effective for membranous nephropathy or multiple sclerosis, and we await the renal and neurologic response.

Discussion

Alemtuzumab depletes B and T lymphocytes and can produce side effects associated with immune reconstitution, with thyroid toxicity seen in up to 30% of patients. However, nephrotoxicity is rare (5/1485 patients, 0.3%). Mechanisms underlying kidney-related side effects from alemtuzumab use are not fully understood but may be linked to the anti-CD52 immunomodulatory effect on B and T cell lymphocytes. The autoimmune diseases observed after administering alemtuzumab are predominantly antibody-mediated and appear to respond to B-cell depletion, suggesting that rituximab may be a potentially effective therapy.