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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.
Cardiac arrhythmias are common in CKD and may accelerate renal function decline via heart–kidney crosstalk. Premature ventricular complexes (PVCs), the most frequent ventricular ectopy and prevalent in CKD, may impair renal perfusion and reduce cardiac output, while CKD promotes PVCs through electrolyte imbalance, fibrosis, and uremia. High PVC burden has been linked to ventricular dysfunction, but its impact on kidney outcomes remains unclear. This multicenter study aimed to determine whether high PVC burden independently predicts accelerated kidney function decline in patients with advanced CKD.
In this multicenter, retrospective cohort study, 1,804 CKD stage 3–4 patients from two tertiary hospitals in Taiwan (2009–2021) who underwent 24-hour Holter monitoring were analyzed. Patients were enrolled from Taiwan’s pre-End-Stage Renal Disease (pre-ESRD) integrated care program, a nationwide multidisciplinary management initiative providing standardized follow-up and laboratory monitoring for patients. High PVC burden was defined as >30/hr (>720/day). The primary outcome was a kidney-specific composite of sustained ≥40% eGFR decline or end-stage kidney disease (sustained eGFR <10 mL/min/1.73 m² or dialysis initiation). The secondary outcome additionally included all-cause mortality. Associations between PVC burden and outcomes were assessed using multivariable Cox regression, Fine–Gray competing risk models, and propensity score–matched analyses, adjusting for demographics, comorbidities, baseline kidney function, and chronic medications.
Over a median follow-up of 4.2 years, 695 patients (39%) reached the primary renal outcome. After comprehensive adjustmentt for demographic factors, baseline kidney function, comorbidities, and chronic medication use, high PVC burden remained independently associated with increased risk of the primary composite event (HR 1.35, 95% CI 1.09–1.66, p = 0.005), the secondary composite including mortality (HR 1.28, 95% CI 1.08–1.51, p = 0.004), and greater annual eGFR decline (−2.53 vs. −1.68 mL/min/1.73 m²/year, p < 0.001). Each log-unit increase in daily PVC count conferred higher renal risk (HR 1.08, 95% CI 1.02–1.15). Findings were consistent across competing risk and propensity score–matched analyses, with no significant effect modification across subgroups. When modeled as a continuous variable, each log-unit increase in daily PVC count was linearly associated with higher renal risk (HR 1.08, 95% CI 1.02–1.15).
High PVC burden is independently associated with accelerated kidney function decline and increased risk of renal failure in patients with CKD. These findings highlight PVCs as a potentially modifiable arrhythmic marker contributing to cardiorenal progression, supporting early rhythm assessment and intervention in CKD care. A preliminary version of this work was presented as a poster at ASN Kidney Week 2025 (Abstract 4349959, Houston, TX).
