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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.
Endogenous digitalis-like cardiotonic steroids (CTS), i.e., inhibitors of Na and K-ATPase, were first considered important in the regulation of renal sodium transport and arterial pressure. Recent studies have implicated CTS in cell growth and fibrosis and in the pathogenesis of chronic kidney disease (CKD). Marinobufagenin (MBG) is a CTS that induces fibrosis through a mechanism involving Fli1, a negative regulator of collagen-1 synthesis, in accordance with our previous studies in rats with subtotal nephrectomy and preeclampsia. Human MBG levels are significantly increased in end-stage CKD. In small mammals with MBG-induced cardiac fibrosis, the mineralocorticoid antagonist (MRA) spironolactone blocked the profibrotic effects of MBG in the absence of changes in aldosterone levels. Our hypothesis was that MRA may lower MBG levels and therefore the aim was to investigate the effect of MRA on MBG levels in patients with CKD using spironolactone (Spiro) and compare the results with those not using spironolactone (nSpiro).
A prospective cross-sectional study was conducted at the University Hospital, which included 19 consecutive patients with CKD and 8 healthy controls (HC). Plasma MBG levels and various laboratory parameters (serum creatinine, S-Creat, µmol/l; estimated glomerular filtration rate, eGFR, ml/min, etc.) and clinical indicators (systolic blood pressure – SBP, AGEs, advanced glucation end-products using an AGE counter) were assessed. Plasma MBG was measured using an ELISA test. Data were processed using the Statistica (version 13.5.0.17) software package. The study was approved by the Human Research Ethics Committee of the University of Tartu (protocol 391/M-15, 2024).
Consecutive CKD patients were divided into two groups: 10 patients in the Spiro group (mean age 83 ± 8.3 years, eGFR 50 ± 9.5 m/min, SBP 131.0 ± 17.6) and 9 patients in the nSpiro group (mean age 75.6 ± 11.7 years, eGFR 26.1 ± 11.8 ml/min, SBP 146.1 ± 17.1). Plasma MBG correlated with the levels of two profibrotic factors, procollagen-1 terminal peptide (p = 0.029) and FGF-23 (p = 0.021). The mean plasma MBG concentration was significantly (p = 0.04) lower in the Spiro group (190.0 ± 19.4 Pg/ml) compared to nSpiro patients (216.4 ± 38.4 Pg/ml) or HC subjects (205.0 ± 28.3 Pg/ml).
The study showed that MRA treatment in patients with CKD was associated with a decrease in MBG levels in the blood and lower blood pressure. These data suggest that elevated MBG levels may be associated with the development of arterial fibrosis.
The results of the estudy have been partially presented at the 2025 annual conference of the Faculty of Medicine of the University of Tartu.
