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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) patients, especially those with diabetic kidney disease (DKD), carry a significantly elevated risk of cardiovascular disease (CVD) and mortality. DKD, a major microvascular complication of diabetes, induces both glomerular and tubular injury, leading to progressive renal dysfunction and often culminating in end-stage renal disease (ESRD). The pathophysiological mechanisms linking kidney injury and cardiovascular dysfunction, often termed cardiorenal syndrome (CRS), involve complex molecular pathways including RAAS overactivation, inflammation, oxidative stress, and endothelial dysfunction. Although the increased cardiovascular risk in DKD is established, the detailed characterization of cardiac function deterioration in relation to CKD progression by diabetic etiology remains incompletely elucidated. This study aims to explore cardiovascular markers' influence on CKD progression and examine differences between DKD and non-diabetic CKD cohorts.
We conducted a retrospective cohort study spanning 10 years at the University of Virginia Health Services, USA. The study involved 4042 CKD patients stratified by diabetic etiology (1886 had DKD, while 2156 were non diabetic CKD). Renal progression was assessed by serial measurements of creatinine, estimated glomerular filtration rate (eGFR), and blood urea nitrogen (BUN). Cardiac function was evaluated using echocardiographic parameters(all the patients had echocardiography), including left ventricular ejection fraction (LVEF) and the E/e′ ratio as an indicator of diastolic function. Comparisons were made between the DKD and non-diabetic CKD groups. Statistical analysis employed nonparametric tests, regression modeling, Spearman correlation, ANOVA, and K-means clustering to identify predictors of rapid CKD progression and associated cardiovascular changes.
The DKD cohort exhibited significantly faster renal function decline versus non-diabetic CKD (p < 0.001). Regression analysis revealed that older age (p < 0.001), elevated systolic blood pressure (p = 0.026), and lower baseline hemoglobin (p = 0.001) significantly predicted eGFR decline. Worsening renal function correlated with deteriorating cardiac diastolic (E/e′ ratio, r = -0.075, p < 0.01) and systolic (LVEF, r = 0.078, p < 0.01) function, with longitudinal trends confirming significant increases in creatinine, BUN, and E/e′ ratio over time (p < 0.001); however, LVEF remained relatively stable. Racial disparities in eGFR decline were identified (p < 0.001), while lifestyle factors such as smoking and alcohol use were not significant predictors. Logistic regression modeling for rapid CKD progression was significant (χ² = 31.48, p < 0.001), with age as the main predictor.
Diabetes substantially accelerates CKD progression, closely linked to progressive cardiac dysfunction, reinforcing a strong cardiorenal interplay that defines CRS pathophysiology. Hypertension and anemia emerge as critical therapeutic targets. These findings emphasize the imperative for integrated cardiorenal risk management strategies, particularly focusing on DKD patients, to mitigate progression towards ESRD and adverse cardiovascular outcomes.
