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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.
Podocyte depletion due to a congenital low podocyte endowment and/or acquired podocyte loss, represents a common final pathway in most progressive glomerular diseases. Urinary podocyte markers provide a non-invasive method to quantify podocyte loss from glomeruli. Although urinary excretion of podocyte markers has been well studied in patients with chronic kidney disease (CKD), data in young adults without CKD remain scarce. In this study, we examined the urinary podocalyxin levels in Australian indigenous Aboriginal people, who are reported to have a lower nephron number and a higher incidence of kidney failure.
Urine samples and data were obtained from two life-course studies in northern Australia: the Aboriginal Birth Cohort (indigenous) and the Top End Cohort (non-indigenous). Participants with evidence of CKD (urinary albumin excretion ≥30 mg/g and/or eGFR <60 mL/min/1.73 m²) were excluded. Urinary podocalyxin levels were measured using a commercially available ELISA, and their associations with clinical factors and neonatal status were examined.
The urinary levels of podocalyxin were measured in 433 participants with a mean age of 25.3 years. Of these participants, 233 (54%) were female, and 333 (77%) were indigenous. A history of small for gestational age (SGA) was identified in 64 (15 %) participants. The median urinary podocalyxin level was 2.5 (IQR 1.2–4.7) μg/g, showing a right-skewed distribution. Higher urinary podocalyxin excretion was associated with female sex, non-indigenous, higher birth weight, absence of SGA history, lower BMI, less current smoking, and greater albuminuria. In contrast, blood pressure, eGFR, and diabetes status were not significantly associated with urinary podocalyxin. Multivariable linear regression analysis revealed that non-indigenous and higher urinary albumin excretion remained independently associated with higher urinary podocalyxin excretion after adjusting for sex, SGA history, and smoking status.
This is the first community-based study to evaluate urinary podocyte markers in young adults without apparent CKD. Our results suggest that subclinical podocyte injury, as indicated by albuminuria within the normal range, and genetic or racial factors, such as nephron number or total podocyte number per kidney, are both associated with urinary podocalyxin excretion. Further longitudinal studies are needed to determine the significance of urinary podocyte markers in predicting the incidence of CKD.
