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Recurrent focal segmental glomerulosclerosis (FSGS) following kidney transplantation presents a significant clinical challenge, often leading to graft dysfunction and poor long-term outcomes. Early recognition and timely intervention are crucial to preserving graft function, yet atypical presentations can complicate timely diagnosis. This report describes an unusual early recurrence of FSGS in a kidney transplant recipient, characterized by post-transplant anuria, and highlights the diagnostic and therapeutic complexities associated with this condition.
Case Presentation
A 24-year-old male with end-stage renal disease (ESRD) secondary to primary focal segmental glomerulosclerosis (FSGS), diagnosed in 2017, presented for kidney transplantation in 2024. He had been maintained on hemodialysis for two years prior to receiving a living-related kidney transplant from his mother (HLA 0-0-0 mismatch; donor blood group O-negative, recipient A-positive). Pre-transplant evaluation revealed no donor-specific antibodies (DSAs), negative crossmatches, and a cytomegalovirus (CMV) mismatch (D+/R–), for which he was initiated on valacyclovir prophylaxis.
The operation was uneventful. Postoperatively, the patient initially demonstrated excellent graft function, with a urine output of 600–800 mL/hour and steadily improving serum creatinine. However, by postoperative day (POD) 2, urine output progressively declined, and he became completely anuric despite normal resistive indices and patent renal vessels on Doppler ultrasound.
By POD 16, urine output gradually resumed. At that time, the urine protein-to-creatinine ratio (UPCR) ranged between 8–11 g/g, and serum albumin was 3.1 g/dL. Electron microscopy subsequently revealed diffuse (100%) podocyte foot-process effacement, confirming the diagnosis of early recurrent FSGS (Figures 1 and 2). The patient underwent a total of 12 plasmapheresis sessions and received a single dose of Obinutuzumab, along with maintenance of higher tacrolimus trough levels and discontinuation of sirolimus.
At the most recent follow-up, the patient maintained stable graft function, with a serum creatinine of 0.9 mg/dL, improved proteinuria (UPCR 1 g/g), and normalization of serum albumin (4.2 g/dL).
Discussion
Recurrent FSGS remains a diagnostic and therapeutic challenge in kidney transplantation, with up to 30–50% of cases experiencing early recurrence. This case is distinctive for its atypical, early presentation with complete anuria, occurring in the absence of histologic features of rejection or significant vascular compromise. Such a presentation can obscure the diagnosis, as early recurrence typically manifests with abrupt nephrotic-range proteinuria rather than anuric graft dysfunction. The delayed confirmation of recurrent FSGS—achieved only through electron microscopy (EM) demonstrating diffuse podocyte foot-process effacement—highlights the critical diagnostic value of EM, especially when light microscopy findings are inconclusive.
Therapeutic strategies for recurrent FSGS remain largely empirical, as no standardized regimen has been universally accepted. Reported treatments include plasmapheresis, rituximab, Obinutuzumab, and other B-cell– or complement-targeted therapies. Responses are variable, and relapses are common, underscoring the need for an individualized approach guided by disease severity, recurrence timing, and treatment response. In this case, early initiation of plasmapheresis combined with Obinutuzumab and optimization of calcineurin inhibitor levels resulted in significant recovery of graft function and improvement in proteinuria.
This case highlights the diagnostic challenges of early, aggressive recurrence of primary FSGS following kidney transplantation, where anuria may be the only presenting feature, likely secondary to acute tubular injury induced by heavy proteinuria and circulating permeability factors.
Electron microscopy plays a pivotal role in confirming the diagnosis, especially when light microscopy fails to reveal glomerular pathology.
A multidisciplinary approach, incorporating early clinical suspicion, prompt diagnostic evaluation, and individualized immunomodulatory therapy, remains essential to optimizing graft outcomes in recurrent FSGS post-transplantation.
