Recurrence of IgA nephropathy in a kidney transplant patient successfully treated with iptacopan—a case report

IgA nephropathy recurrence after kidney transplantation is a common complication, which is most often detected histologically. Recurrence after transplant affects long-term graft survival, with prognosis being worse with increasing levels of proteinuria, a higher histological activity, and concurrent rejection. Treatment in kidney transplant patients is similar to that in native kidneys: using renin–angiotensin–aldosterone system (RAAS) blockade agents, steroids, and increased immunosuppression. Iptacopan, an inhibitor of alternative complement pathway factor B, has demonstrated reduction in proteinuria and complement activity in native IgAN. However, it has not been studied in recurrent IgAN after kidney transplant. We present a case of recurrent IgAN refractory to conventional therapy with clinical and histological improvement after treatment with iptacopan. A 39-year-old male patient underwent a deceased donor kidney transplantation. A 3-month biopsy showed features of recurrent IgAN in the transplanted kidney. Following treatment for rejection, subsequent biopsies demonstrated active IgAN with worsening proteinuria, which was treated with rituximab, cyclophosphamide, and steroids. Despite these interventions, there was no improvement in IgAN or proteinuria. At 40 months post-transplant, the patient was started on iptacopan, after which a follow-up biopsy showed resolution of active IgA activity. The patient has tolerated iptacopan well and has not had any adverse events or serious infections.