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• W4315706943 abstract "Objective: Hypertensive disorders of pregnancy (HDP) are a leading cause of maternal and infant morbidities and mortalities. Activity of the renin angiotensin aldosterone system (RAAS) is critical for the physiology of pregnancy, and suppressed RAAS during pregnancy is associated with adverse outcomes, such as preeclampsia. Obesity is a major contributor to adverse outcomes of pregnancy, and obesity modulates the RAAS in non-pregnant conditions. It is not known how the RAAS is regulated with obesity during pregnancy. We quantified serum biomarkers of the classical and alternative arms of the RAAS in a cohort of pregnant women to determine associations between obesity and activity of the RAAS during pregnancy. Design and Methods: We recruited a prospective cohort of n = 36 pregnant women in the first trimester with no clinical risk factors. Patients were separated into two groups, greater (n = 23) or less than (n = 13) body mass index (BMI) of 30 kg/m2 at enrollment. We quantified 6 angiotensin peptides, aldosterone, and enzyme activities of ACE2 and NEP in serum using LC-MS/MS in the first and third trimester. PRA, S was calculated as: Ang I + Ang II (pmol/L). Data are median [IQR]. Results: PRA, S and aldosterone increased with pregnancy in both groups, but the change from first to third trimester was reduced in the BMI > 30 group compared to those with BMI < 30 (PRA-S: 24.1 [-45.4 to 194.7] versus 70.9 [9.2 to 113.1]) pmol/L, respectively; Aldo: 234.3 [45.5 to 532.7] versus 648.2 [182.1 to 1207.3] pmol/L, respectively; P < 0.05). ACE2 activity was increased during pregnancy, with no differences between groups, however, NEP activity was elevated in the BMI > 30 group at both time points during pregnancy compared to the BMI < 30 group (1st trim: 13.4 [8.1 to 20.38] versus 8.4 [3.7 to 12.03]; 3rd trim: 21.3 [11.7 to 26.5] versus 13.47 [10.5 to 22.8] ng/mL; P < 0.01). In the BMI < 30 group, n = 2 developed gestational hypertension and n = 1 developed postpartum preeclampsia. In contrast, in the BMI > 30 group, n = 7 developed gestational hypertension, n = 2 developed preeclampsia/postpartum preeclampsia. Conclusion: Activity of the classical RAAS is reduced in women with 1st trimester BMI > 30 compared to those with BMI < 30. In contrast, the alternative RAS is not suppressed by obesity during pregnancy. Further, elevated 1st trimester BMI was associated with more adverse outcomes. Reduced activity of the classical RAAS with obesity may contribute to adverse outcomes in pregnancy." @default.
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• W4315706943 date "2023-01-01" @default.
• W4315706943 modified "2023-10-17" @default.
• W4315706943 title "PS-C30-10: EFFECT OF OBESITY ON SERUM PROFILES OF THE RENIN ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS) IN PREGNANCY" @default.
• W4315706943 doi "https://doi.org/10.1097/01.hjh.0000917656.06874.01" @default.
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