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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
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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.
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Abstract titles should be brief and reflect the content of the abstract.
In a prior CKD S1-5 cohort (N=1,213; 48% male; age 48±16 years), echocardiographic features of left ventricular hypertrophy were independently associated with serum phosphate (Pi). To elucidate mechanisms linking Pi dysregulation to cardiovascular remodeling in mild CKD-MBD, we conducted translational study.
Experimental CKD was induced in adult male spontaneously hypertensive rats (SHRs) via 3/4 nephrectomy (Nx) with a 4-month follow-up; sham-operated SHRs (SO) were controls. Animals received standard chow (0.6% phosphorus). We assessed: renal function (serum creatinine, proteinuria, interstitial fibrosis); cardiovascular parameters (systolic blood pressure, myocardial mass index); serum biomarkers (sPi, PTH, FGF23); tissue analysis (myocardial/bone phosphorus, bone histomorphometry, cardiac remodeling); molecular pathways: PiT1 (Slc20a1), PiT2 (Slc20a2), and phospho-ERK1/2 (Mapk3/1) expression (RT-qPCR, Western blot, IHC with quantitative morphometry, confocal microscopy). Clinical Study enrolled 78 patients with biopsy-proven immune glomerulopathies (CKD S1–4; 52% male; age 43 ± 13), excluding extrarenal diseases and immunosuppressive therapy. Control group: healthy subjects of corresponding age and gender (n=10). Evaluations included: cardiac function (echocardiography, NT-proBNP); phosphate metabolism (serum Pi, renal Pi excretion indices, 25OHD, PTH, FGF23, Klotho); bone turnover (osteocalcin, bone/total ALP, β-CrossLaps).
Experimental kidney injury exhibited features of human CKD2, lower bone turnover (↓osteoblasts, osteocytes numbers, eroded perimeter). SPi, myocardial P content were higher in the Nx group vs SO, without significant differences in 24-hour urinary Pi excretion, bone P content, PTH, FGF23. In CKD-MBD, bone Slc20a1 and Mapk1 expression were lower (Figure1A) with a reduction in PiT1 and phospho-ERK1/2 IHC staining (Figure1B). Myocardial P accumulation, fibrosis, cardiomyocyte hypertrophy were associated with higher Slc20a2 and Mapk3 mRNA, PiT2 protein, phosphorylated ERK1/2 expressions (Figure2).
In clinical study Pi and FEPi were independently (vs biomarkers) associated with ECHO parameters of cardiac remodeling. Mild CKD have already had ↑LVMI with ↓25OHD3 and osteocalcin, suggesting osteoblast suppression with defective mineralization (Figure3). Moderate to severe CKD showed obvious cardiac remodeling with mineral disturbances – rising PTH, β-CrossLaps, BAP with persistent low 25OHD, osteocalcin (Figure3).
Bone and myocardium responses to Pi retention are already apparent in mild CKD. Clinical findings suggest lower bone turnover progressing to secondary hyperparathyroidism. Experimental data implicate PiT1/2 and ERK1/2 pathway may underlie tissue remodelling in mild CKD-MBD highlight a new therapeutic target before PTH/FGF23 elevation.
