Vascular Biomarkers Predictive of the Progression From Hypertensive Disorders in Pregnancy to Preeclampsia in Pregnant Women
NCT ID: NCT04520048
Last Updated: 2025-09-12
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
RECRUITING
Clinical Phase
NA
Total Enrollment
110 participants
Study Classification
INTERVENTIONAL
Study Start Date
2023-08-11
Study Completion Date
2026-12-31
Brief Summary
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Hypertension during pregnancy remains a leading cause of maternal and fetal morbidity and mortality. The frequency (5 to 10% of pregnancies) and potential severity of these diseases, both for the mother and the child, are reasons for standardizing and optimizing medical practices.
The cause of hypertension during pregnancy is quite complex, as it depends on a number of factors. Among the hypertensive disorders in pregnancy (HDP), the pathophysiology of pre-eclampsia (one of the most studied in terms of severity) remains poorly understood. The evolution of international guidelines in recent years has made it possible to distinguish various HDP, but schematically we distinguish two main entities by the existence of proteinuria from and after the 20th week of amenorrhea and by maternal-fetal complications, more serious in pre-eclampsia than in gestational hypertension.
Acute placental vasculature and blood flow abnormalities were observed during gestational hypertension and preeclampsia, and maybe due to generalized vascular endothelial activation and vasospasm resulting in systemic hypertension and organ hypoperfusion. Endothelial dysfunction (ED) and abnormal expression of several specific blood biomarkers are now well accepted as characteristics of preeclampsia as a leader.
However, the progression of any HDP to preeclampsia is possible, but difficult to predict. By way of example, among between 15 and 40 % of gestational hypertension cases progress to preeclampsia, suggesting that it is the same worsening disease.
ED could be pre-existing (chronic, white-coat or masked hypertension) but also at the origin of gestational hypertension (unclassified hypertension, transient pregnancy hypertension), and subsequent development of preeclampsia through an imbalance between pro- and anti-angiogenic factors.
An imbalance of pro-angiogenic and anti-angiogenic proteins can testify to ED, as can adequate levels of endothelial microparticles.
The main objective of this research is to assess the presence of urinary endothelial microparticles in stable pregnant women with hypertensive disorder of pregnancy as a marker for the occurrence of pre-eclampsia during pregnancy.
The cause of hypertension during pregnancy is quite complex, as it depends on a number of factors. Among the hypertensive disorders in pregnancy (HDP), the pathophysiology of pre-eclampsia (one of the most studied in terms of severity) remains poorly understood. The evolution of international guidelines in recent years has made it possible to distinguish various HDP, but schematically we distinguish two main entities by the existence of proteinuria from and after the 20th week of amenorrhea and by maternal-fetal complications, more serious in pre-eclampsia than in gestational hypertension.
Acute placental vasculature and blood flow abnormalities were observed during gestational hypertension and preeclampsia, and maybe due to generalized vascular endothelial activation and vasospasm resulting in systemic hypertension and organ hypoperfusion. Endothelial dysfunction (ED) and abnormal expression of several specific blood biomarkers are now well accepted as characteristics of preeclampsia as a leader.
However, the progression of any HDP to preeclampsia is possible, but difficult to predict. By way of example, among between 15 and 40 % of gestational hypertension cases progress to preeclampsia, suggesting that it is the same worsening disease.
ED could be pre-existing (chronic, white-coat or masked hypertension) but also at the origin of gestational hypertension (unclassified hypertension, transient pregnancy hypertension), and subsequent development of preeclampsia through an imbalance between pro- and anti-angiogenic factors.
An imbalance of pro-angiogenic and anti-angiogenic proteins can testify to ED, as can adequate levels of endothelial microparticles.
The main objective of this research is to assess the presence of urinary endothelial microparticles in stable pregnant women with hypertensive disorder of pregnancy as a marker for the occurrence of pre-eclampsia during pregnancy.
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Detailed Description
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Hypertension in pregnancy is defined by PAS ≥140 mmHg and/or PAD ≥ 90 mmHg, mild to moderate hypertension by PAS = 140-159 mmHg and/or PAD = 90-109 mmHg and severe hypertension by PAS ≥ 160 mmHg and/or PAD ≥ 110 mmHg.
Definitions of hypertensive disorders in pregnancy have evolved considerably. We know that during gestational hypertension (GE) there is no pathologic elevation of proteinuria (after 20 weeks of amenorrhea). Preeclampsia (PE) is defined as high blood pressure (controlled or uncontrolled) associated with proteinuria discovered after the 20th week of amenorrhea.
The cause of hypertension and pathophysiology during pregnancy and in particular of preeclampsia remains poorly understood. Endothelial dysfunction and abnormal blood levels of several biomarkers are associated with PE, such as: soluble Fms-like- tyrosine kinase 1 (sFlt-1), Placental Growth Factor (PIGF) and Vascular Endothelial Growth Factor (VEGF). VEGF is of particular importance due to its direct vasodilating effect at systemic level through its interaction with nitric oxide (NO). There is a bi-directional regulation between VEGF and NO, which has direct implications for endothelium, capillary permeability and angiogenesis. sFlt-1 (circulating form of VEGF receptor) has the property of neutraliting the growth factors VEGF and PIGF. Inhibition of VEGF has a known biological effect on endothelial function in adults and is believed to be a key factor in explaining elevated blood pressure. This has been demonstrated in patients undergoing anti-angiogenic therapy in combination with chemotherapy. Other biomarkers of preeclampsia are less known and could be involved in pathophysiological mechanisms; mainly hypervolemia, renal dysfunction and activation of inflammation. The progression of gestational hypertension to preeclampsia is difficult to predict; between 15 and 40 % of gestational hypertension cases progress to preeclampsia, suggesting that it is a single worsening disease. Preeclampsia is known to be one of the few diseases in which acute placental abnormalities manifest at the mother's vascular and renal system levels. These abnormalities are attributable to generalized vascular endothelial activation and vasospasm, resulting in hypertension and hypoperfusion of organs.
Endothelial dysfunction could be at the origin of HDP as gestational hypertension, and subsequently itself contribute to the subsequent development of severe forms such preeclampsia through an imbalance between pro- and anti-angiogenic factors likely in relation with increased oxidative stress.
It is now accepted that angiogenic biomarkers (such as soluble fms-like tyrosine kinase 1, Placenta growth factor and soluble endoglin) contribute to endothelial dysfunction through VEGF antagonizing among others. The dosage of these angiogenic biomarkers in the maternal bloodstream is highly predictive and significantly abnormal from the 23th week of amenorrhea on average, and with a maximum peak between the 32th and 36th week of amenorrhea.
Endothelial microparticles (EMPs) are involved in intracellular communication and produced in normal pregnancy and in PE. The renal damage associated with PE and the potential role of extracellular vesicles are in the main adverse mechanisms that distinguish the different types of hypertension in pregnancy.
Adequate levels of circulating endothelial microparticles (CEMP), circulating endothelial cells (CECs), and endothelial progenitor cells most likely play an important role in the development and regulation of the vasculature during pregnancy, but the exact role in the pathogenesis of PE is unknown.
These endothelial microparticles (EMPs) reflects systemic endothelial damage and can also be measured in urine by flow cytometry. In general, in hypertensive patients, there is peritubular capillary loss (PCL) and it can be measured by these EMPs. Urinary (not blood) MP levels correlate directly with renal hypoxia and fibrosis and inversely with cortical perfusion. Therefore, the level of EMPs could be useful as "new biomarkers" of intrarenal capillary loss. However, only a few in-depth studies in the field of hypertension in pregnancy have focused on this issue.
The main objective is to assess whether the presence of urinary endothelial microparticles (UEMP) in the pregnant woman in a stable condition with discovery of HDP is a marker of the occurrence of preeclampsia later during pregnancy.
The investigators further explore a possible correlation of alteration of UEMP to other biomarkers of pre-eclampsia endothelial dysfunction and vascular involvement in pregnancy hypertension.
Definitions of hypertensive disorders in pregnancy have evolved considerably. We know that during gestational hypertension (GE) there is no pathologic elevation of proteinuria (after 20 weeks of amenorrhea). Preeclampsia (PE) is defined as high blood pressure (controlled or uncontrolled) associated with proteinuria discovered after the 20th week of amenorrhea.
The cause of hypertension and pathophysiology during pregnancy and in particular of preeclampsia remains poorly understood. Endothelial dysfunction and abnormal blood levels of several biomarkers are associated with PE, such as: soluble Fms-like- tyrosine kinase 1 (sFlt-1), Placental Growth Factor (PIGF) and Vascular Endothelial Growth Factor (VEGF). VEGF is of particular importance due to its direct vasodilating effect at systemic level through its interaction with nitric oxide (NO). There is a bi-directional regulation between VEGF and NO, which has direct implications for endothelium, capillary permeability and angiogenesis. sFlt-1 (circulating form of VEGF receptor) has the property of neutraliting the growth factors VEGF and PIGF. Inhibition of VEGF has a known biological effect on endothelial function in adults and is believed to be a key factor in explaining elevated blood pressure. This has been demonstrated in patients undergoing anti-angiogenic therapy in combination with chemotherapy. Other biomarkers of preeclampsia are less known and could be involved in pathophysiological mechanisms; mainly hypervolemia, renal dysfunction and activation of inflammation. The progression of gestational hypertension to preeclampsia is difficult to predict; between 15 and 40 % of gestational hypertension cases progress to preeclampsia, suggesting that it is a single worsening disease. Preeclampsia is known to be one of the few diseases in which acute placental abnormalities manifest at the mother's vascular and renal system levels. These abnormalities are attributable to generalized vascular endothelial activation and vasospasm, resulting in hypertension and hypoperfusion of organs.
Endothelial dysfunction could be at the origin of HDP as gestational hypertension, and subsequently itself contribute to the subsequent development of severe forms such preeclampsia through an imbalance between pro- and anti-angiogenic factors likely in relation with increased oxidative stress.
It is now accepted that angiogenic biomarkers (such as soluble fms-like tyrosine kinase 1, Placenta growth factor and soluble endoglin) contribute to endothelial dysfunction through VEGF antagonizing among others. The dosage of these angiogenic biomarkers in the maternal bloodstream is highly predictive and significantly abnormal from the 23th week of amenorrhea on average, and with a maximum peak between the 32th and 36th week of amenorrhea.
Endothelial microparticles (EMPs) are involved in intracellular communication and produced in normal pregnancy and in PE. The renal damage associated with PE and the potential role of extracellular vesicles are in the main adverse mechanisms that distinguish the different types of hypertension in pregnancy.
Adequate levels of circulating endothelial microparticles (CEMP), circulating endothelial cells (CECs), and endothelial progenitor cells most likely play an important role in the development and regulation of the vasculature during pregnancy, but the exact role in the pathogenesis of PE is unknown.
These endothelial microparticles (EMPs) reflects systemic endothelial damage and can also be measured in urine by flow cytometry. In general, in hypertensive patients, there is peritubular capillary loss (PCL) and it can be measured by these EMPs. Urinary (not blood) MP levels correlate directly with renal hypoxia and fibrosis and inversely with cortical perfusion. Therefore, the level of EMPs could be useful as "new biomarkers" of intrarenal capillary loss. However, only a few in-depth studies in the field of hypertension in pregnancy have focused on this issue.
The main objective is to assess whether the presence of urinary endothelial microparticles (UEMP) in the pregnant woman in a stable condition with discovery of HDP is a marker of the occurrence of preeclampsia later during pregnancy.
The investigators further explore a possible correlation of alteration of UEMP to other biomarkers of pre-eclampsia endothelial dysfunction and vascular involvement in pregnancy hypertension.
Conditions
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Hypertension Disorders in Pregnancy
Gestational Hypertension
Pre-Eclampsia
Study Design
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Allocation Method
NA
Intervention Model
SINGLE_GROUP
Primary Study Purpose
PREVENTION
Blinding Strategy
NONE
Study Groups
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Women with a hypertension disorder in pregnancy and/or preeclampsia
Pregnant patients from the 20th week of amenorrhea with the initial diagnosis of a hypertension disorder in pregnancy and/or preeclampsia. Patients in a stable state undergoing follow-up consultation (day hospital and week hospitalization)
Group Type
EXPERIMENTAL
Determination of the UEMP levels
Intervention Type
OTHER
Quantification of UEMP by flow cytometry in urine (10 ml) collected at 26 ± 2 week and 34th ± 2 week of amenorrhea.
Aortic central pressure and the carotid-femoral pulse wave velocity
Intervention Type
PROCEDURE
Measurement of the aortic central arterial pressure (systolic and diastolic arterial pressure) by applanation tonometry, and the index of aortic increase by applanation tonometry, the carotid-femoral pulse wave velocity using the SphygmoCor® system (PWV Medical) and/or Popmetre.
Vascular biomarker assay
Intervention Type
OTHER
Plasma angiogenic biomarker levels determination using an immunoassay, including circulating sFlt-1, circulating PIGF, sFlt-1 / PIGF ratio, circulating VEGF, circulating soluble endoglin (sEng), other biomarkers assessment, including anti-angiotensin II receptor (AT1), circulating copeptin, circulating interleukin 17 (IL-17), Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL), as well as CEMP and CEC quantification using flow cytometry.
Measurement of the uterine artery diameter
Intervention Type
PROCEDURE
This measurement is added to the routine examination of the uterine artery. Bi-dimensional ultrasound imaging with angio-Doppler allows the study of the artery as the blood flow velocity and vessel diameter. Uterine artery Doppler pulsatility index (UtA-PI), mean flow velocity and diameter measurement could be calculated with Doppler instrument with software could determine instantaneous true mean blood flow velocity. Measurement is made by placing the cursor from outer edge to outer edge of the artery adventitia, on a cross-section and taking the largest diameter
Interventions
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Determination of the UEMP levels
Quantification of UEMP by flow cytometry in urine (10 ml) collected at 26 ± 2 week and 34th ± 2 week of amenorrhea.
Intervention Type
OTHER
Aortic central pressure and the carotid-femoral pulse wave velocity
Measurement of the aortic central arterial pressure (systolic and diastolic arterial pressure) by applanation tonometry, and the index of aortic increase by applanation tonometry, the carotid-femoral pulse wave velocity using the SphygmoCor® system (PWV Medical) and/or Popmetre.
Intervention Type
PROCEDURE
Vascular biomarker assay
Plasma angiogenic biomarker levels determination using an immunoassay, including circulating sFlt-1, circulating PIGF, sFlt-1 / PIGF ratio, circulating VEGF, circulating soluble endoglin (sEng), other biomarkers assessment, including anti-angiotensin II receptor (AT1), circulating copeptin, circulating interleukin 17 (IL-17), Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL), as well as CEMP and CEC quantification using flow cytometry.
Intervention Type
OTHER
Measurement of the uterine artery diameter
This measurement is added to the routine examination of the uterine artery. Bi-dimensional ultrasound imaging with angio-Doppler allows the study of the artery as the blood flow velocity and vessel diameter. Uterine artery Doppler pulsatility index (UtA-PI), mean flow velocity and diameter measurement could be calculated with Doppler instrument with software could determine instantaneous true mean blood flow velocity. Measurement is made by placing the cursor from outer edge to outer edge of the artery adventitia, on a cross-section and taking the largest diameter
Intervention Type
PROCEDURE
Eligibility Criteria
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Inclusion Criteria
* Patients with a hypertension disorder in pregnancy and/or preeclampsia from the 20th amenorrhea week until the 26th ± 2 amenorrhea week.
* Age between 18 and 40 years old.
* Having given written consent.
* Patients affiliated to a social security scheme.
* Age between 18 and 40 years old.
* Having given written consent.
* Patients affiliated to a social security scheme.
Exclusion Criteria
* Presence of pathologies interfering in a major way with vascular parameters: known multicomplicated diabetes treated before pregnancy, hypercholesterolemia known (or LDL\>130 mg/dl), multicomplicated connectivitis, proven cardiovascular disease (ischemic heart disease, stroke, arteriopathy of the lower limbs, heart failure), pre-existing known renal failure (serum creatinine \>125 µmol/L) and/or pre-existing proteinuria ≥ 300 mg/24h).
* Cardiac arrhythmia.
* Hepatitis C, HIV infection (assay performed within 6 months prior to diagnosis of pre-eclampsia).
* Recent history of venous (pulmonary embolism, phlebitis) or arterial (myocardial infarction, unstable angina, stroke, transient ischemic attack), thrombotic event ≤ 3 months.
* Patient already engaged in a therapeutic protocol.
* Patients under legal protective measures.
* Patients receiving State Medical Assistance.
* Cardiac arrhythmia.
* Hepatitis C, HIV infection (assay performed within 6 months prior to diagnosis of pre-eclampsia).
* Recent history of venous (pulmonary embolism, phlebitis) or arterial (myocardial infarction, unstable angina, stroke, transient ischemic attack), thrombotic event ≤ 3 months.
* Patient already engaged in a therapeutic protocol.
* Patients under legal protective measures.
* Patients receiving State Medical Assistance.
Minimum Eligible Age
18 Years
Maximum Eligible Age
40 Years
Eligible Sex
FEMALE
Accepts Healthy Volunteers
No
Sponsors
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Assistance Publique - Hôpitaux de Paris
OTHER
Sponsor Role
lead
Responsible Party
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Responsibility Role
SPONSOR
Principal Investigators
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Marilucy LOPEZ-SUBLET, MD
Role: PRINCIPAL_INVESTIGATOR
AP-HP Avicenne Hospital, Department of Internal Medicine, ESH Hypertension European Excellence Centre
Locations
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AP-HP Avicenne Hospital, Department of internal medicine
Bobigny, Seine Saint Denis, France
Site Status
RECRUITING
AP-HP Jean Verdier Hospital, Gynecology and Obstetrics Department
Bondy, Seine Saint Denis, France
Site Status
RECRUITING
AP-HP Laribosière Hospital, Gynecology and Obstetrics Department
Paris, , France
Site Status
RECRUITING
Countries
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France
Central Contacts
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Facility Contacts
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References
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Thomopoulos C, Hitij JB, De Backer T, Gkaliagkousi E, Kreutz R, Lopez-Sublet M, Marketou M, Mihailidou AS, Olszanecka A, Pechere-Bertschi A, Perez MP, Persu A, Piani F, Socrates T, Stolarz-Skrzypek K, Cifkova R. Management of hypertensive disorders in pregnancy: a Position Statement of the European Society of Hypertension Working Group 'Hypertension in Women'. J Hypertens. 2024 Jul 1;42(7):1109-1132. doi: 10.1097/HJH.0000000000003739. Epub 2024 Apr 11.
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Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
2019-A03207-50
Identifier Type: OTHER
Identifier Source: secondary_id
APHP200237
Identifier Type: -
Identifier Source: org_study_id
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