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Abstract: PO1603

Rituximab for Severe Recurrent Proliferative Lupus Nephritis After Kidney Transplantation: Pondering a Rare Case

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Song, Rui, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • He, Mingyue, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Rakhman, Ilay, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Constantinescu, Serban, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
  • Lee, Iris J., Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, United States
Introduction

Severe histologic recurrence of lupus nephritis (LN) post-kidney transplant(KTX) is extremely rare on standard transplant immunosuppression. Severe recurrence shortens allograft survival, yet treatment guidelines post-KTX are lacking.

Case Description

A 52-year-old African American (AA) man with ESRD secondary to LN underwent a second KTX from a deceased donor. He had a prior living-unrelated KTX with graft failure due to mixed rejection without LN recurrence. For the second KTX, he received Thymoglobulin induction and maintenance immunosuppressive regimen: Enteric-coated mycophenolate sodium (EC-MPS), Tacrolimus, Prednisone, with immediate graft function (nadir creatinine 1.4mg/dL). He developed leukopenia requiring a reduction of EC-MPS to 360mg twice daily. He developed nephrotic range proteinuria 6 months post-KTX but had stable allograft function, bland urine sediment, normal complements, and negative anti-dsDNA antibodies. Despite inactive serologies, allograft biopsy revealed diffuse proliferative sclerosing and crescentic LN (ISN/RPS class IV). Due to persistent leukopenia, Rituximab was chosen over commonly-used Cyclophosphamide (CYC) for therapy. He received intravenous Methylprednisolone (3000 mg) and Rituximab 800mg (375 mg/m2) for 4 doses. Complete B-cell depletion was maintained for 3 months. His proteinuria decreased from 6.9 g/g to 1.2 g/g, and renal allograft function remained stable.

Discussion

Severe recurrent LN post-kidney transplant is rare and can present atypically. Negative serologic markers, bland urine sediment and lack of LN recurrence on the first KTX did not rule out LN recurrence on the second kidney allograft. In our case, only the presence of persistent progressive proteinuria warranted allograft biopsy. AA ethnicity and reduction of EC-MPS were risk factors, which highlights the significance of full transplant maintenance therapy to prevent recurrent LN. B cell plays a pivotal role in LN pathogenesis. Rituximab targets CD20+ B cells and has been successfully utilized for refractory LN. It has a more favorable toxicity profile compared to CYC which has been the conventional treatment for clinically significant LN post-KTX. We propose Rituximab as a better treatment option for severe recurrence of LN post-KTX.