ArticleScientific reports2026
Circulating levels of sFlt-1 and AT1-AA in women with prior preeclampsia: a 10-year postpartum cross-sectional analysis (PERLA-Brazil study).
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study investigated whether soluble fms-like tyrosine kinase-1 (sFlt-1) and angiotensin II type 1 receptor autoantibodies (AT1-AA) - key mediators of preeclampsia (PE) pathophysiology - remain elevated ten years postpartum, thereby contributing to the long-term cardiovascular disease (CVD) risk in women with a history of PE. In a retrospective cohort nested within the PERLA-Brazil project, 205 women were enrolled: 103 with a documented history of PE (PH group) and 102 with normotensive pregnancies (NH group). Participants completed standardized interviews, underwent physical evaluations, and provided blood samples for sFlt-1 and AT1-AA quantification by enzyme-linked immunosorbent assay (ELISA), alongside comprehensive clinical and demographic data collection. No significant differences were observed in circulating sFlt-1 (90.25 ± 6.11 pg/mL in PH vs. 93.30 ± 5.54 pg/mL in NH, p = 0.886) or AT1-AA levels (6.80 ± 0.16 ng/mL in PH vs. 6.34 ± 0.18 ng/mL in NH, p = 0.060) between groups a decade after the index pregnancy. Clinical and biochemical data were collected and compared between groups, with multivariable models adjusted for age, body mass index, and educational attainment. As results, it was observed that women with severe PE history had higher systolic and diastolic blood pressure, higher low-density lipoprotein cholesterol, and a greater prevalence of hypertension. These findings suggest that the long-term cardiovascular burden after PE is not explained by increased plasma levels of sFlt-1 or AT1-AA, but may instead reflect durable downstream vascular and metabolic remodeling. The study underscores PE as a marker of future cardiovascular vulnerability and highlights the need to identify additional mechanisms and biomarkers underlying this risk.This highlights PE as an early-life stressor with persistent effects and underscores the need of lifelong CVD prevention strategies for affected women, as well as the importance of identifying additional biological or physiological markers associated with their sustained risk.
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