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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.
Primary aldosteronism (PA) accounts for 5–10% of patients with hypertension and is the most common form of secondary hypertension. Compared to essential hypertension, PA is associated with a higher risk of cerebro-cardiovascular complications, which is thought to be attributable to elevated plasma aldosterone levels. Recent evidence (Nakano E, et al. Endocr J. 2024) suggests that the high plasma aldosterone concentration (PAC) response to adrenocorticotropic hormone (ACTH) stimulation may be associated with a history of cerebro-cardiovascular events in patients with PA. However, the clinical significance of high PAC response to ACTH stimulation in PA patients remains unclear. This study aimed to investigate the relationship between the PAC response to ACTH stimulation and various clinical parameters in patients with PA.
We conducted a cross-sectional analysis of 42 patients who were diagnosed with PA by functional tests and underwent adrenal venous sampling (AVS) with ACTH stimulation between April 2015 and October 2024. All clinical parameters were assessed during hospitalization for AVS. During this period, all patients were placed on a salt-restricted diet containing 6 grams of sodium. AVS was performed on the morning of the third day of hospitalization. PAC was measured at baseline after 30 minutes of supine rest, using blood samples collected via catheter from the inferior vena cava. ACTH stimulation was performed during AVS, and additional blood samples were collected one hour after the ACTH load. The percentage change in PAC was calculated as follows: (PAC after ACTH – PAC before ACTH) / PAC before ACTH × 100.
The percentage change in PAC following ACTH stimulation demonstrated a statistically significant positive correlation with the urinary N-acetyl-β-D-glucosaminidase to creatinine ratio (NAG/Cre) (R = 0.356, p = 0.024), indicating a potential association with renal tubular injury. In contrast, the percentage change in PAC was negatively correlated with the ankle-brachial index (ABI) and serum creatinine levels (R = -0.444, p = 0.003, R = -0.350, p = 0.023).
In patients with PA, a higher PAC response to ACTH stimulation was associated with elevated renal damage markers and lower ABI values. The association between PAC change and serum creatinine levels may reflect glomerular hyperfiltration, which is consistent with previous studies. These findings suggest that the PAC response to ACTH stimulation could serve as a potential indicator of organ damage in patients with primary aldosteronism, and prospective longitudinal studies are warranted to clarify this point.
