Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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) represents a unique phenotype characterized by accelerated vascular remodeling, contributing to both atherosclerosis and arteriosclerosis following vascular calcification. Early kidney damage—manifested as alterations in the glomerular filtration barrier—is difficult to detect. Albuminuria is a globally accepted method for early detection; however, other urinary proteins and peptides may also serve as early markers of cardiorenal syndrome and vascular remodeling.
Here, we hypothesize that urinary biomarkers are associated with central hemodynamics—systolic (cSBP) and diastolic (cDBP) pressure—and vascular remodeling, measured as carotid-femoral pulse wave velocity (cfPWV), in a diabetes-free, healthy population.
Subjects from the Malmö Offspring Study (MOS) cohort with available plasma creatinine, plasma cystatin C, and urinary samples were randomly selected for urine aliquots. The Human ProcartaPlex™ Kidney Toxicity Panel 1 (Luminex assay) was used to measure 11 protein targets in a single well (se the table below). The urinary albumin-to-creatinine ratio (UACR) was also determined. The urinary protein-to-creatinine ratio (protein/Cr) was used to account for variations in urine concentration. Additionally, individuals with hypertension (n = 34) were compared with non-hypertensive participants (n = 118). Hypertension was defined as peripheral blood pressure higher than 140/90 mmHg.
Protein Name
Abbreviation
Calbindin
Clusterin
Apolipoprotein J
Glutathione S-transferase A1
GSTA1
Interleukin-18
IL-18
Interferon-inducible protein 10
IP-10 / CXCL10
Kidney Injury Molecule-1
KIM-1 / TIM-1 / HAVCR1
Monocyte Chemoattractant Protein-1
MCP-1 / CCL2
Osteoactivin
GPNMB
Retinol-binding Protein 4
RBP4
Renin
Vascular Endothelial Growth Factor A
VEGF-A
A total of 152 individuals (mean age 41 ± 6 years; 42% female) were analyzed. cSBP was negatively correlated with the urinary IL-18/Cr ratio (r = –0.198, p = 0.046); this relationship was slightly stronger than that observed with UACR (r = 0.195, p = 0.046). Central diastolic blood pressure (cDBP) was positively associated with the urinary KIM-1/Cr ratio (r = 0.227, p = 0.025), but not with UACR. Urinary VEGF-A, RBP4, GSTA1, and Calbindin values were significantly associated with cSBP (rs = 0.234, p = 0.004; rs = 0.212, p = 0.010; rs = 0.225, p = 0.018; and rs = 0.184, p = 0.023, respectively). Urinary GSTA1 values were also correlated with cDBP (rs = 0.194, p = 0.042). No associations were found between cfPWV and any of the urinary proteins. Individuals with hypertension had higher urinary KIM-1/Cr levels (p = 0.047), but no differences in UACR.
This study supports the utility of urinary proteins beyond UACR as early indicators of changes in central hemodynamics and hypertension but not aortic stiffness.
