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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.
Chronic kidney disease (CKD) and hypertension (HTN) are known risk factors for cardiovascular (CV) morbimortality in the general population. The consequences of CKD and HTN on childhood cancer survivors’ (CCS) morbimortality is unknown. The aim of this study was to determine the extent to which incident CKD and HTN in CCS are associated with mortality with major adverse cardiovascular events (MACE).
This population-based retrospective cohort study used administrative healthcare data from Ontario, Canada. We included patients diagnosed from April 1993 to March 2020 who started treatment at age <18 years old and who survived to end of cancer therapy (index date). Patients with pre-diagnosis of organ transplant, dialysis, past malignancy, HTN or CKD were excluded. The primary exposures were CKD or HTN, defined by previously validated diagnosis and procedure codes. The primary outcome was the development of MACE. Secondary outcomes were the individual components of MACE (cardiovascular death, stroke, myocardial infarction (MI), unstable angina (UA) hospitalization, and coronary intervention) and all-cause mortality. Multivariable Cox regression analysis was used to determine the association between CKD and HTN exposures and MACE, coded as time-varying covariates where an individual becomes ‘exposed’ at first evidence of CKD/HTN during follow-up. Cox proportional hazards models were used to model the association between CKD/HTN as time varying covariates on outcomes. For the analysis of MACE and MACE composites, death was considered a competing event.
10,182 CCS were included (median follow-up 9.8 years [interquartile range 3.8 -17.2]. Patients were censored for end of follow-up (6,890, 67.7%), new cancer diagnosis/relapse (1,683, 16.5%) or emigration (439, 4.3%). Death occurred in 562 cases (5.5%) and MACE in 608 (6.0%) of the total population. CKD was associated with an adjusted risk of 2.56 (95% confidence interval [CI] 1.73, 3.79) times for MACE, while HTN was associated with an adjusted risk of 1.72 (95% CI 1.23, 2.42) (Table 1). Both CKD and HTN individually were associated with increased risk for CV death (adjusted hazard ratio [aHR] 12.47, CI 6.87-22.65 and aHR 3.29, CI 1.54-7.00), stroke (aHR 2.24, CI 1.30-3.84 and aHR 1.62, CI 1.02-2.56), coronary intervention (aHR 12.43, CI 3.15-49.13 and aHR 12.47, CI 3.41-45.55) and all-cause mortality (aHR 4.26, CI 3.09-5.88 and aHR 1.59, CI 1.07-2.37), and an increased risk for MI or UA with CKD (aHR 2.15, CI 1.08-4.28). The associations of CKD with MACE and HTN with MACE were not modified by sex (interaction p-value 0.50), age (interaction p-value 0.45), and acute kidney injury(interaction p-value 0.68).
Both CKD and HTN were associated with an increased risk of MACE in CCS. Current gaps in clinical guidelines highlight the need for evidence-based recommendations on long-term monitoring of CCS, as our findings linking CKD and HTN to increased MACE risk suggest potential benefits from early detection and management.