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Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Although immunosuppressive agents are expected to be effective in anti-nephrin antibody-positive FSGS, recurrence after kidney transplantation can occur even with B-cell depletion therapy, suggesting the possibility of antibody production by plasma cells. This paper reports on a case of FSGS recurrence after transplantation treated with CD38 monoclonal antibody.
A 35-year-old male developed nephrotic syndrome in April and underwent a renal biopsy. Foam cells and focal segmental glomerulosclerosis were observed. IgG colocalized with nephrin was stained, leading to a diagnosis of anti-nephrin antibody-positive FSGS. Treatment with steroids, rituximab (RTX), and LDL apheresis, but treatment was unsuccessful. Hemodialysis started on July 13, and the patient was admitted to the hospital on November 7 for living donor kidney transplantation.In addition to RTX, Basiliximab, mycophenolate mofetil, and tacrolimus, as well as plasma exchange and IVIG. A kidney transplant was performed on November 22. On postoperative day 2, Cre improved to 1.3 mg/dL, but gradually increased from postoperative day 5 and did not respond to additional plasma exchange and steroid therapy. Proteinuria remained unchanged before and after surgery, at approximately 15 g/day. Hemodialysis was required from postoperative day 21, and a transplant kidney biopsy was performed on postoperative day 32. The biopsy showed tubulointerstitial inflammation and negative C4d deposition with intraluminal proliferation, leading to a diagnosis of FSGS recurrence.
Dara was administered on postoperative days 34 and 53, but it was unsuccessful and renal function was lost.
Although immunosuppressive agents are expected to be effective in anti-nephrin antibody-positive FSGS, relapse after transplantation can occur even following B-cell depletion therapy with RTX, suggesting the possibility of antibody production by plasma cells. In this case, Dara, an anti-CD38 monoclonal antibody, was administered with the expectation that it would suppress plasma cell-derived antibody production, but it was ineffective. This may be due to the already lost renal function or the possibility of antibody leakage via low-selectivity proteinuria. Japan Renal Transplantation Physician Association
