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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.
Normal pregnancy induces significant hemodynamic changes, including increased cardiac output, blood volume expansion due to sodium and water retention, and reduced systemic vascular resistance. However, it remains unclear how to accurately assess renal function during pregnancy using serum creatinine or cystatin C.
This observational cohort study included 4,513 healthy pregnant women with at least two serum creatinine measurements (pre-pregnancy and during pregnancy) for analyzing absolute and relative changes in creatinine. A separate group of 1,613 healthy pregnant women with at least two serum cystatin C measurements (pre-pregnancy and during pregnancy) was included for the analysis of cystatin C changes. We evaluated the association between changes in biomarkers (creatinine or cystatin C) during pregnancy and adverse pregnancy outcomes (APOs), both before and after model adjustment. APOs were defined as the occurrence of any of the following: preeclampsia, eclampsia, HELLP syndrome, gestational hypertension, gestational diabetes mellitus (GDM), preterm delivery (gestational age < 37 weeks), obstructed labor, or miscarriage.
In women with healthy renal function, creatinine levels decreased from early pregnancy, reaching a nadir (10.6 μmol/L lower than pre-pregnancy levels, a 20.7% reduction) at 26–28 weeks of gestation, and subsequently returned to pre-pregnancy levels. Cystatin C levels also declined from early pregnancy, reached a nadir (0.169 mg/L lower than pre-pregnancy, a 21.6% reduction) around 18 weeks, returned to pre-pregnancy levels by approximately 28 weeks, and then increased further to 0.159 mg/L above pre-pregnancy levels (a 21.1% increase) before gradually declining to baseline after delivery. Restricted cubic spline (RCS) analysis revealed that the ratio of pregnancy-to-pre-pregnancy creatinine was not significantly associated with APOs before adjusting for its physiological changes; however, after adjustment, a higher ratio was significantly associated with an increased risk of APOs. Compared to women with creatinine fluctuations between 0.6 and 1.4 times the baseline, a 40% increase in creatinine during pregnancy was associated with a 21% higher risk of APOs (hazard ratio [HR] = 1.21, 95% confidence interval [CI]: 1.05–1.39). Cystatin C exhibited a similar trend: its pregnancy-to-pre-pregnancy ratio showed no significant association with APOs before adjustment, but a higher adjusted ratio was significantly associated with an increased APO risk. Compared to women with cystatin C fluctuations between 0.6 and 1.4 times the baseline, a 40% increase in cystatin C during pregnancy was associated with a 24% higher risk of APOs (HR = 1.24, 95% CI: 1.08–1.42).
We developed a novel model for assessing renal function during pregnancy. After model adjustment, longitudinal changes in creatinine or cystatin C serve as significant risk factors for APOs.
