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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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Cancer patients receiving chemotherapy are at risk of developing a wide spectrum of drug-induced kidney injuries. Among these, drug-induced thrombotic microangiopathy (TMA) is a particularly challenging entity, often leading to chronic kidney dysfunction. It may be difficult to distinguish drug-induced TMA from other primary TMAs, and the principal treatment is withdrawal of the causative drug, which requires early recognition.
We report the case of a 52-year-old woman with metastatic ovarian serous adenocarcinoma who developed biphasic kidney dysfunction during chemotherapy with bevacizumab and pegylated liposomal doxorubicin (PLD). The patient was diagnosed with ovarian cancer nine years earlier and underwent hysterectomy, oophorectomy, colectomy, and adjuvant paclitaxel–carboplatin therapy. Two years before the current presentation, her regimen was switched to bevacizumab, and PLD was added seven months prior to admission. At one year before admission, she developed new-onset proteinuria and mild kidney dysfunction. Suspecting drug-induced nephrotoxicity, bevacizumab was discontinued; however, renal dysfunction persisted, prompting a kidney biopsy.
Light microscopy demonstrated a membranoproliferative glomerulonephritis pattern, endothelial injury at interlobular artery to arteriole level and a partially present PAS-positive hyaline pseudothrombi. No significant immune deposits were observed on immunofluorescence. Electron microscopy revealed vacuolated material in the subendothelial space, suggesting the involvement of PLD.
Based on the temporal relationship with drug initiation, lack of renal recovery after withdrawal of bevacizumab, and characteristic pathological findings, the biphasic kidney-limited TMA was attributed to both agents: endothelial injury initially caused by bevacizumab followed by additive drug-induced TMA triggered by PLD. TMA associated with PLD has been rarely reported, but its distinctive pathological features were evident in this case. Importantly, kidney-limited TMA is likely under-recognized despite being relatively frequent, particularly in oncology patients.
This case highlights the importance of careful clinicopathological correlation for the early diagnosis of drug-induced kidney-limited TMA in patients with malignancy. Recognition of characteristic renal histopathological findings is crucial in differentiating drug-induced TMA from other etiologies. Timely diagnosis allows prompt cessation of the offending drug, which may preserve kidney function and optimize patient outcomes during chemotherapy.
