Long-term renal and cardiovascular risk after preeclampsia: towards screening and prevention

Paauw, Nina D.; Luijken, Kim; Franx, Arie; Verhaar, Marianne C.; Lely, A. Titia

doi:10.1042/cs20150567

Cited by 77 publications

(66 citation statements)

References 73 publications

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“…Complement consumption in PE through the classical pathway is supported by an increasing body of evidence finding enhanced complement breakdown products in a variety of tissue samples in PE 32,[39][40][41][42][43][44][45][46][47]. Women with PE have a higher risk of developing renal and cardiovascular disease in the future 50. The elevated polyclonal sFLC levels in this study were independent of markers of inflammation and renal function, supporting a humoral response in PE.…”

supporting

confidence: 62%

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Humoral immunity in late‐onset Pre‐eclampsia and linkage with angiogenic and inflammatory markers

Sarween

Drayson

Hodson

et al. 2018

American J Rep Immunol

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supporting

confidence: 62%

“…48,49 Women with PE have a higher risk of developing renal and cardiovascular disease in the future. 50 Further studies are required to determine the time course of the rise in sFLC levels in PE and whether this also exists prepregnancy.…”

Section: Discussionmentioning

confidence: 99%

Humoral immunity in late‐onset Pre‐eclampsia and linkage with angiogenic and inflammatory markers

Sarween

Drayson

Hodson

et al. 2018

American J Rep Immunol

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“…Preeclampsia (PE) is a major pregnancy complication characterized by hypertension and proteinuria (1) and is the second most common cause of maternal morbidity (2)(3)(4). Epidemiologic studies indicate that a history of PE correlates with the later development of cardiovascular disease (5). Although both maternal and placental factors contribute to its pathogenesis, the etiology of PE is incompletely understood.…”

mentioning

confidence: 99%

Decreased LIN28B in preeclampsia impairs human trophoblast differentiation and migration

Canfield¹,

Arlıer²,

Mong³

et al. 2018

FASEB j.

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Preeclampsia (PE) is a common cause of maternal morbidity, characterized by impaired trophoblast invasion and spiral artery transformation resulting in progressive uteroplacental hypoxia. Given the primary role of LIN28A and LIN28B in modulating cell metabolism, differentiation, and invasion, we hypothesized that LIN28A and/or LIN28B regulates trophoblast differentiation and invasion, and that its dysregulation may contribute to PE. Here we show that LIN28B is expressed ∼1300‐fold higher than LIN28A in human term placenta and is the predominant paralog expressed in primary human trophoblast cultures. The expression of LIN28B mRNA and protein levels are significantly reduced in gestational age–matched preeclamptic vs. normal placentas, whereas LIN28A expression is not different. First trimester human placental sections displayed stronger LIN28B immunoreactivity in extravillous (invasive) cytotrophoblasts and syncytial sprouts vs. villous trophoblasts. LIN28B overexpression increased HTR8 cell proliferation, migration, and invasion, whereas LIN28B knockdown in JEG3 cells reduced cell proliferation. Moreover, LIN28B knockdown in JEG3 cells suppressed syncytin 1 (SYN‐1), apelin receptor early endogenous ligand (ELABELA), and the chromosome 19 microRNA cluster, and increased mRNA expression of ITGp4and TNF‐α. Incubation of BeWo and JEG3 cells under hypoxia significantly decreased expression of LIN28B and LIN28A, SYN‐1, and ELABELA, whereas TNF‐α is increased. These results provide the first evidence that LIN28B is the predominant paralog in human placenta and that decreased LIN28B may play a role in PE by reducing trophoblast invasion and syncytialization, and by promoting inflammation.—Canfield, J., Arlier, S., Mong, E. F., Lockhart, J., Vanwye, J., Guzeloglu‐Kayisli, O., Schatz, F., Magness, R. R., Lockwood, C. J., Tsibris, J. C. M., Kayisli, U. A., Totary‐Jain, H. Decreased LIN28B in preeclampsia impairs human trophoblast differentiation and migration. FASEB J. 33, 2759–2769 (2019). http://www.fasebj.org

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“…The risk of a woman in the developing world dying from a maternal-related cause is 33 times higher than a woman in the developed world 16. Maternal mortality results from cerebral hemorrhage,17 pulmonary edema,18 acute renal failure, hepatic rupture, or DIC. Long-term effects may include chronic renal failure, cardiovascular disease,19 or cortical blindness.…”

Section: Discussionmentioning

confidence: 99%

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

Ngwenya¹

2017

IJWH

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BackgroundSevere preeclampsia is a disorder of pregnancy characterized by high blood pressure and significant proteinuria after 20 weeks gestation. Severe preeclampsia and eclampsia have considerable adverse impacts on maternal, fetal, and neonatal health especially in low-resource countries. Hypertensive disorders of pregnancy are the third leading cause of maternal deaths in Sub-Saharan Africa. Significant avoidable maternal and neonatal morbidity and mortality may result.ObjectivesThis study aimed 1) to determine the incidence of severe preeclampsia/eclampsia in a low-resource setting; 2) to determine the maternal complications of severe preeclampsia/eclampsia in a low-resource setting; 3) to determine the perinatal outcomes of severe preeclampsia/eclampsia in a low-resource setting.MethodsThis was a retrospective descriptive cohort study carried out at Mpilo Central Hospital, a tertiary teaching referral government hospital in a low-resource setting in Bulawayo, Zimbabwe. Data were obtained from the birth registers in labor ward, intensive care unit, and neonatal intensive care unit of patients who had a diagnosis of severe preeclampsia or eclampsia for the period January 1, 2016, to December 31, 2016. The case notes were retrieved and the demographic, clinical, and outcome data were gathered.ResultsThere were 9,086 deliveries at the institution during the period January 1, 2016, to December 31, 2016. There were 121 cases of severe preeclampsia/eclampsia. The incidence of severe preeclampsia/eclampsia was 1.3% at Mpilo Central Hospital. The most common major complication was HELLP syndrome (9.1%). Maternal mortality was 1.7%. There were 127 babies born with six sets of twins, 49.6% of the babies were lost through stillbirths and early neonatal deaths.ConclusionThe incidence of severe preeclampsia/eclampsia at Mpilo Central Hospital was 1.3%. The most common maternal complication was hemolysis elevated liver enzymes low platelet syndrome. Maternal mortality was 1.7% due to acute renal failure. Nearly half (49.6%) of the babies born were lost to stillbirths and early neonatal deaths.

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Long-term renal and cardiovascular risk after preeclampsia: towards screening and prevention

Cited by 77 publications

References 73 publications

Humoral immunity in late‐onset Pre‐eclampsia and linkage with angiogenic and inflammatory markers

Humoral immunity in late‐onset Pre‐eclampsia and linkage with angiogenic and inflammatory markers

Decreased LIN28B in preeclampsia impairs human trophoblast differentiation and migration

Severe preeclampsia and eclampsia: incidence, complications, and perinatal outcomes at a low-resource setting, Mpilo Central Hospital, Bulawayo, Zimbabwe

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