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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.
Imatinib, a tyrosine kinase inhibitor(TKI) targeting platelet-derived growth factor receptor (PDGFR), BCR-ABL and c-KIT, is generally regarded as a well-tolerated agent. However, prolonged inhibition of PDGFR signaling can lead to endothelial dysfunction and causes thrombotic microangiopathy (TMA) in rare cases. We report a case of chronic TMA that developed after 17 years of low-dose imatinib therapy for chronic myeloid leukemia (CML), emphasizing the potential for cumulative endothelial injury associated with extended exposure.
A man in his seventies with hypertension and history of long duration smoking presented with progressive bilateral leg edema. He had been treated with imatinib 100 mg/day for 17 years for CML. On admission, blood pressure was 144/81mmHg. Urinary analysis revealed Up/Uc 4.81g/gCrand blood test revealed renal dysfunction with eGFR 52.3mL/min/1.73㎡. Chest X-ray and ECG showed no abnormalities, and renal ultrasound revealed preserved kidney size and cortical thickness. A renal biopsy was performed for further evaluation.
Light microscopy revealed focal mesangiolysis, mesangial expansion, and double-contour formation of the glomerular basement membrane in glomeruli. Arterioles demonstrated marked fibrous intimal thickening and hyaline change. Immunofluorescence showed non-specificIgM positivity limited to the mesangial areas, without other immune-complex deposition. Electron microscopy demonstrated subendothelial widening consistent with chronic TMA. The absence of alternative causes and the histological findings strongly suggested imatinib-induced endothelial injury. As discontinuation of imatinib could lead to poor prognosis for CML, we have decided to continue Imatinib. Though massive proteinuria continued, no worsening of renal function was observed.
This case highlights that long-term exposure to low-dose imatinib can induce chronic TMA through sustained PDGFR inhibition, particularly in patients with vascular risk factors such as hypertension, smoking, and aging. To our knowledge, This case represents the longest reported interval between initiation of Imatinib therapy and the onset of TMA. Previous reports on VEGF inhibitors and other TKIs have suggested a relationship between cumulative drug exposure and the development of TMA. In the present case, the relatively low dose of Imatinib (100 mg/day) might have contributed to the unusually long latency before onset of TMA.
