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Abstract: PO1885

A Case of IgA Nephropathy in the Setting of Sezary Syndrome and Mogamulizumab

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Doraiswamy, Mohankumar, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Brodsky, Sergey V., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Reneau, John C., The Ohio State University Comprehensive Cancer Center Arthur G James Cancer Hospital and Richard J Solove Research Institute, Columbus, Ohio, United States
  • Leisring, Joshua, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States

IgA Nephropathy (IgAN) is an autoimmune disease with complex pathogenesis. Sezary syndrome (SS) is a leukemic subtype of cutaneous T cell lymphoma (CTCL). A rare association has previously been reported between IgAN and CTCL. Mogamulizumab (MG) is a monoclonal antibody drug targeting C-C chemokine receptor type 4 (CCR4) and is used in the treatment of CTCL and SS. MG has been associated with drug eruptions and systemic immune-mediated adverse events.

Case Description

A 63 year-old woman with SS was treated with MG. Her skin symptoms improved and circulating Sezary cells cleared. Due to a cutaneous drug eruption, the frequency of MG administration was reduced to monthly after cycle 7. Labs prior to cycle 19 demonstrated serum creatinine (Cr) 1.77 mg/dL from a prior baseline ~0.9-1.0 mg/dL. She received intravenous fluids but Cr worsened to 3.97 mg/dL. Urinalysis (UA) revealed more than 20 red blood cells (RBCs) per high powered field (HPF). 24 hour urine protein to creatinine ratio (UPCR) was 2.03 g/g. Serologies and complements were normal except double stranded DNA which was 12 IU/mL (normal <4 IU/mL). Kidney biopsy demonstrated mesangial immune complex deposition with IgA, IgG, and C3 predominance consistent with IgAN (Oxford M1E0S1T1C0). Prednisone was initiated at 1 mg/kg/day and tapered over 6 months. MG was stopped. After 6 months Cr had improved to 1.10 mg/dL. UA showed 3-5 RBCs per HPF with UPCR of 0.122 g/g. Her SS remained well controlled without systemic therapy.


This case reinforces the association between IgAN and CTCL which has been described in prior case series. In patients with CTCL, altered T cell populations and a dysregulated immune response may contribute to the pathogenesis of IgAN. Complicating this case is the use of MG which can deplete normal CCR4-expressing regulatory T cells by inducing antibody-dependent cellular cytotoxicity. MG is associated with cutaneous granulomatous drug eruptions in which alterations in T cell populations have been implicated. Systemic autoimmune complications outside of the kidneys have also been reported. The possibility that MG could play a role in IgAN should be considered.