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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
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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Abstract titles should be brief and reflect the content of the abstract.
Recurrent focal segmental glomerulosclerosis (rFSGS) is a cause of allograft dysfunction with detrimental outcomes. We report a case of a kidney transplant recipient who developed rFSGS 26 years after transplantation, after undergoing microwave ablation (MWA) of hepatocellular carcinoma (HCC).
A 63-year-old man with End Stage Renal Disease (ESRD) due to presumed ‘chronic glomerulonephritis’ received a living-related kidney donation from his sister in 1999. There was immediate graft function, but he developed oliguria and allograft dysfunction with serum creatinine rising from 216 to 456 µmol/L on post-operative day 4. Allograft biopsy revealed cytoplasmic vacuolation but no evidence of acute rejection. He was treated empirically for rFSGS with methylprednisolone and plasma exchange, with improvement in the serum creatinine down to 130 µmol/L and resolution of proteinuria.
He developed multiple post-transplant malignancies including squamous cell carcinoma of the finger in January 2018, native renal cell carcinoma in July 2018, and hepatocellular carcinoma in April 2025, and he was put on cyclosporin A, everolimus and prednisolone as immunosuppression. His proteinuria increased from 0.5 g/day to 1.1 g/day in August 2023 but he refused renal biopsy; with decrease back to 0.5g/day after stopping everolimus. His serum creatinine and proteinuria levels remained stable afterwards.
He presented with sudden-onset nephrotic syndrome (proteinuria 10 g/day, serum albumin 17 g/L) in May 2025 after undergoing microwave ablation of the HCC one month before. An allograft biopsy found rFSGS. He underwent seven sessions of plasma exchange and received rituximab, achieving a good clinical response with urine proteinuria dropping to 0.5g/day. Serum creatinine remained between 150-160 µmol/L, which was close to his baseline.
We postulate that MWA induced coagulative necrosis of the HCC resulted in a surge of inflammatory mediators leading to production of permeability factor and subsequent podocyte injury. This circulating factor-mediated mechanism is supported by the patient’s favourable clinical response to plasma exchange. This case highlights the importance of monitoring for potential rFSGS triggered after procedures inducing significant tissue necrosis and inflammation.
