Childhood growth outcomes 2 years after hypertensive versus normotensive pregnancy: a p4 study

ABSTRACT BACKGROUND Intrauterine exposure to hypertensive disorders of pregnancy, including gestational hypertension (GH) and preeclampsia (PE), may influence infant growth and have

long-term health implications. This study aimed to compare growth outcomes of infants exposed to a normotensive pregnancy (NTP), GH, or PE from birth to 2 years. METHODS Infants were

children of women enroled in the prospective Postpartum Physiology, Psychology and Paediatric (P4) cohort study who had NTP, GH or PE. Birth, 6-month (age-corrected) and 2-year

(age-corrected) weight z-scores, change in weight z-scores, rapid weight gain (≥0.67 increase in weight z-score) and conditional weight gain z-scores were calculated to assess infant growth

(NTP = 240, GH = 19, PE = 66). RESULTS Infants exposed to PE compared to NTP or GH had significantly lower birth weight and length z-scores, but there were no differences in growth outcomes

at 6 months or 2 years. GH and PE-exposed infants had significantly greater weight z-score gain [95% CI] (PE = 0.93 [0.66–1.18], GH = 1.03 [0.37–1.68], NTP = 0.45 [0.31–0.58], _p_ < 0.01)

and rapid weight gain (GH = 63%, PE = 59%, NTP = 42%, _p_ = 0.02) from birth to 2 years, which remained significant for PE-exposed infants after confounder adjustment. CONCLUSION In this

cohort, GH and PE were associated with accelerated infant weight gain that may increase future cardiometabolic disease risk. IMPACT * Preeclampsia exposed infants were smaller at birth,

compared with normotensive pregnancy and gestational hypertension exposed infants, but caught up in growth by 2 years of age. * Both preeclampsia and gestational hypertension exposed infants

had significantly accelerated weight gain from birth to 2 years, which remained significant for preeclampsia exposed infants after adjustment for confounders including small for gestational

age. * Monitoring of growth patterns in infants born following exposure to a hypertensive disorder of pregnancy may be indicated to prevent accelerated weight gain trajectories and obesity.

SIMILAR CONTENT BEING VIEWED BY OTHERS PRE-PREGNANCY BODY MASS INDEX, GESTATIONAL WEIGHT GAIN AND POSTNATAL GROWTH IN PRETERM INFANTS Article 19 May 2021 ORAL SODIUM SUPPLEMENTATION ON

GROWTH AND HYPERTENSION IN PRETERM INFANTS: AN OBSERVATIONAL COHORT STUDY Article 05 August 2024 HIGHER BLOOD PRESSURE IN ADOLESCENT BOYS AFTER VERY PRETERM BIRTH AND FETAL GROWTH

RESTRICTION Article Open access 07 November 2022 INTRODUCTION Approximately 5–10% of pregnancies worldwide are complicated by hypertensive disorders of pregnancy (HDP).1 This includes 3–5%

gestational hypertension (GH), characterised by new onset hypertension ≥20 weeks gestation, and 2–5% preeclampsia (PE), where new onset hypertension is associated with maternal organ

dysfunction or foetal compromise.1,2,3,4,5 For affected mothers, GH and PE carry an increased lifetime risk of cardiometabolic diseases including hypertension, ischaemic heart disease,

stroke, and type 2 diabetes.3,5,6,7,8,9,10 PE is also associated with adverse foetal outcomes such as foetal growth restriction (FGR), placental abruption, stillbirth and neonatal mortality.

Approximately 12–33% of PE-exposed neonates are born small for gestational age (SGA).11,12 As delivery is the only definitive treatment for PE,13 many neonates are born preterm (<37

weeks gestation), with associated complications including respiratory distress syndrome and sepsis,6,14,15,16,17 and poorer outcomes are more likely for neonates exposed to early-onset PE

(diagnosis <34 weeks gestation).18,19 While GH alone is associated with less severe perinatal outcomes,20 25% of GH cases develop into PE, with a higher rate in early onset.13,21 In the

long term, intrauterine exposure to HDP has been associated with an increased incidence of cardiometabolic,22,23,24,25 immunological26,27,28,29 and neurodevelopmental30,31,32,33,34,35,36,37

morbidities in children. The Developmental Origins of Health and Disease (DOHaD) hypothesis provides a plausible explanation for the long-term complications seen in children exposed to HDP.

This hypothesis suggests that foetal adaptations to an adverse intrauterine environment, as experienced in HDP, may cause ‘developmental programming’ that increases future risk of morbidity

compared to children of normotensive pregnancies (NTPs).38,39,40 Rapid growth trajectories during infancy may also occur in response to an adverse intrauterine environment, typically

nutrient insufficiency, a phenomenon known as the ‘thrifty phenotype’.41 Such rapid weight gain has been associated with later neurological, cardiovascular, renal and respiratory

morbidity,42,43 as well as an increased risk of obesity and later cardiometabolic dysfunction.44,45,46 Our recent narrative review identified 11 studies assessing growth from birth to

2-years in infants exposed to PE versus NTP.47 Overall, studies reported that PE-exposed infants either had lower weight, length and BMI at 2 years than normotensive controls, or that they

instead experienced accelerated weight gain to catch up in growth by 2 years.47 Combined with these inconsistent findings is the fact that the role of SGA and prematurity status within these

studies was inconsistently explored. For instance, several prior studies were limited to HDP-exposed infants born premature or of very-low-birthweight (VLBW),48,49,50,51 which themselves

are independent risk factors for impaired infant growth.52,53 Further research adjusting for these confounders is required and no prior study has investigated the difference in growth

trajectories in a cohort comprising NTP, GH and PE-exposed infants in the first two years of life. Our previous study54 reported lower absolute weight and weight z-scores in PE exposed

compared with NTP infants at 6 months of age. The present study extends this research by comparing anthropometric growth measures and growth trajectories, including rapid weight gain and

conditional weight gain, in this cohort at 2-years of age following exposure to NTP, GH or PE. Furthermore, we aim to elucidate impacts on anthropometric outcomes independent of SGA and

prematurity status. METHODS STUDY DESIGN This is a sub-study of the prospective, single-centre cohort study, the P4 (Postpartum Physiology, Psychology and Paediatric) follow-up study being

conducted at St. George Hospital, a metropolitan teaching hospital in Sydney, Australia. The study was approved by the Prince of Wales Hospital Human Research Ethics Committee

(HREC/12/POWH395). A detailed study protocol has been published,55 and this study follows published papers reporting maternal outcomes6 and infant growth outcomes54 6 months postpartum.

STUDY POPULATION Participants in this study were infants of P4-participating mothers. Mothers were eligible if they gave birth to a live singleton infant without major congenital

abnormalities between January 2013 and December 2018 and had a good understanding of written and spoken English. Women were excluded from participating in the P4 study if they were pregnant

again at the time of the 6 month postpartum assessment, or if they had pre-existing diabetes, hypertension, renal or any other serious maternal disease prior to the index pregnancy. Written

informed consent for the mother and infant was obtained at study enrolment, which occurred by 6 months postpartum. The P4 study initially recruited 415 women who were grouped based on their

final diagnosis as either NTP (_n_ = 302), GH (_n_ = 23) or PE (_n_ = 90) according to the International Society for the Study of Hypertension in Pregnancy (ISSHP) Guidelines.21 GH was

defined as persistent, new onset hypertension (Blood Pressure (BP) ≥140 mmHg systolic or ≥90 mmHg diastolic) at or after 20 weeks gestation, while PE was new onset hypertension accompanied

by evidence of maternal organ dysfunction including proteinuria, acute kidney injury, liver dysfunction, neurological features, haematological complications, and/or uteroplacental

dysfunction.21 This study includes infants exposed to NTP, GH or PE that had weight recorded at 2 years (Fig. 1). Prematurity status was defined as birth before 37 weeks gestation,21 and SGA

status as a birthweight z-score corrected for sex and gestational age less than −1.28 (corresponding to below the 10th percentile).56,57 DATA COLLECTION Birthweight to the nearest gram and

length to the nearest 0.5 cm were retrieved retrospectively from the mother’s electronic medical record. Weight, length and head circumference were measured at 6 months and weight and head

circumference measured at 2 years, corrected for gestational age at birth, by a paediatrician.58 Weight in kilograms to the nearest one decimal place was measured with the infant lightly

clothed without shoes using digital scales. Recumbent length at 6 months was measured with a measuring tape to the nearest 0.5 cm. Head circumference around the occipitofrontal diameter was

measured with a measuring tape to the nearest millimetre. Maternal sociodemographic information, medical history, birth details and all other details considered covariates, including total

months breastfed, were collected both retrospectively from the mother’s electronic medical record, and prospectively from P4 surveys and study visits at 6 months and 2 years postpartum.

Maternal BP, body composition, and metabolic markers were also collected at these study visits. OUTCOMES As previously described (Gow et al. (2021)54), birth and 6-month weight and length

z-scores were calculated for term infants using the World Health Organisation (WHO) Child Growth Standards,59,60 and for preterm infants using the INTERGROWTH-21st Preterm Postnatal Growth

Standards,61 which allow for the differing pattern of postnatal growth to 6 months that preterm infants experience.61 The INTERGROWTH-21st standards converge with the WHO Child Growth

Standards at 6 months, and thus the WHO standards were used for all infants from 6 months corrected age.59,61 Two-year weight z-scores were calculated for all infants using the WHO Child

Growth Standards.59,60 Secondary measures of longitudinal infant growth calculated from birth to 2 years, and from 6 months to 2 years, included change in weight z-score, rapid weight gain,

defined as an increase in weight z-score ≥0.67,62 and conditional weight gain, which considers the potential confounding of age, sex, birthweight, and regression to the mean on z-score

change. Conditional weight gain is calculated using the standardised residuals from the linear regression of the 2-year versus 6-month, and 2-year versus birthweight z-scores with age and

sex included as covariates. A positive value indicates a faster (and negative value a slower) rate of weight gain compared to the age and sex-adjusted population mean, adjusted for by the

previous measurement to account for possible regression to the mean.54,63,64 COVARIATES Maternal, infant and birth data considered covariates in relation to GH or PE exposure and infant

growth outcomes included: * Maternal data: age, parity, smoking history, gestational diabetes mellitus status, maternal and paternal ethnicity and education, and first trimester, 6-month and

2-year weight, BMI, average systolic and diastolic BPs, Homoeostatic Model Assessment for Insulin Resistance (HOMA-IR) scores and Edinburgh Postnatal Depression Scale (EPDS) scores. * Birth

data: labour onset and mode of birth. * Infant data: sex, birth gestation, prematurity status, SGA status, length of any neonatal intensive care unit or special care nursery (NICU/SCN)

stay, and total months breastfed in the first 2 years. STATISTICAL ANALYSIS Descriptive statistics were used to summarise infant growth outcomes and covariates for the three exposure groups

(NTP, GH or PE). One-way Analysis of Variance tests (parametric continuous data) and Kruskal-Wallis tests (non-parametric continuous data) with Tukey Post-Hoc analysis, and Chi-Square or

Fisher’s Exact tests (categorical data) were used to estimate whether infant growth outcomes and covariates differed between groups. Associations between covariates and infant growth

outcomes (i.e., weight, weight z-scores, z-score changes, rapid-weight-gain and conditional weight gain z-scores) were explored using simple linear regression. Significant associations were

explored in multivariable linear regression, including adjustment for covariates and confounders such as SGA and prematurity status. Subgroup analyses stratified by SGA and prematurity

status were conducted for selected growth outcomes significant in simple regression. Statistical analysis was performed using IBM SPSS Statistics, version 26.0 (Chicago, IL). A _p_ value of

<0.05 was considered statistically significant. RESULTS From the 415 infants enroled in the P4 Study, 325 had a recorded 2-year weight (Fig. 1) and are included in this analysis. Those

without 2-year weights did not differ from those included in the final sample in terms of gestation at birth, birth weight z-score, 6-month weight z-score, maternal age and BMI at 6 months

postpartum and duration of NICU/ SCN stay. Table 1 details the parental demographic and maternal health outcomes of those included in this study. Compared to the NTP group, both GH and PE

mothers had significantly higher systolic and diastolic BPs, HOMA-IR scores and BMI at all time points (except first trimester BMI for the PE group), while GH mothers had significantly

higher weight at all timepoints. Less than one quarter (_n_ = 14) of PE women experienced early onset PE (≤33 weeks), 16 experienced late onset PE (>33 and <37 weeks), 33 experienced

PE at term (≥37 weeks), and 3 experienced PE postpartum. Birth and infant outcomes are described in Table 2. Compared to the NTP group, GH and PE mothers were less likely to experience

spontaneous labour, more likely to deliver via elective or emergency caesarean section, and PE mothers were more likely to have been nulliparous in the index pregnancy. Compared to both the

NTP and GH groups, PE-exposed infants were more likely to be born preterm, SGA and be admitted to a NICU/ SCN. Median duration of all NICU/ SCN admissions was 3 days (interquartile range

18), and ranged in length from 1 to 77 days. Infants from both hypertensive groups were breastfed for a shorter duration than those from NTP. Table 3 details infant growth outcomes after

exposure to NTP, GH or PE. Compared to the NTP or GH groups, PE-exposed infants had lower weight, length and corresponding z-scores at birth (all _p_ < 0.001). There were no significant

differences in growth outcomes between groups at 6 months or 2 years. From 6 months to 2 years however, GH infants had significantly greater weight gain (_p_ = 0.034), but there were no

other significant differences between groups in this period. From birth to 2 years, GH and PE infants experienced significantly greater gains in weight and weight z-scores compared with NTP

infants (Fig. 2), and were 2.4 [95% CI: 0.9–6.2] and 2.0 [1.1–3.5] times, respectively, more likely to experience rapid weight gain. In PE infants, weight gain and weight z-score gain from

birth to 2 years in those exposed to early onset PE was 10.7 ± 1.3 kg and 0.52 ± 0.86, respectively. In PE infants exposed to late/ term/ postpartum weight gain and weight z-score change

from birth to 2 years was 9.8 ± 1.5 kg and 1.04 ± 1.06, respectively. These differences were not statistically significant. When stratifying our cohort, infants born SGA experienced greater

weight z-score gains than those born not SGA (_p_ < 0.001). Similarly, infants born at term experienced greater weight z-score gains than those born preterm (_p_ = 0.002). In infants not

born SGA, PE-exposure remained significantly associated with higher weight z-score gain than NTP-exposed infants (_p_ = 0.023) from birth to 2-years, while GH-exposed infants did not

significantly differ from NTP-exposed infants. In both term and preterm infants, PE-exposed infants had higher weight z-score gains than NTP-exposed infants (term: _p_ < 0.001, preterm:

_p_ = 0.014) (Table 4A, B, Fig. 3A, B). In univariate linear regression, GH and PE exposure, SGA and prematurity status, 6-month maternal systolic and diastolic BPs, nulliparity, induction

of labour and months breastfed to 2 years were all significantly associated with change in weight z-score from birth to 2 years (Supplementary Table 1). Six-month maternal diastolic BP and

induction labour onset were highly associated with other variables significant in univariate linear regression and were subsequently excluded from multivariable regression. Table 5 details

multiple regression models that explore the influence of GH and PE exposure on change in weight z-score from birth to 2 years. When adjusting for SGA status (Model 1), both GH and PE

exposure remained significantly associated with a greater increase in weight z-score compared to NTP exposure. After adjustments for total months breastfed (Model 2) and other maternal and

birth covariates including 6-month maternal systolic BP, nulliparity status and prematurity status (Models 3) and all covariates (Model 4), only PE remained significantly associated with

increases in weight z-score. DISCUSSION In our population of 325 infants, those exposed to PE were smaller at birth, but caught up to both NTP and GH-exposed infants by 6 months and 2 years.

From birth to 2 years, both GH and PE-exposed infants experienced greater gains in absolute weight, weight z-score, and more rapid weight gain, but only PE-exposure remained significantly

associated with this change in weight z-score after adjustment for confounding variables. To our knowledge, we are the first to compare differences in infant growth and trajectories from

birth to 2 years between NTP, GH and PE exposure groups. We found no association between GH or PE exposure and infant weight or weight z-scores at 6 months and 2 years compared with NTP. Our

findings contrast with earlier studies of preterm and/or VLBW infants,48,50,51 and more recent studies in mixed cohorts,54,65 where those exposed to PE had lower absolute weight or weight

z-scores throughout infancy. Martikainen et al.49 also reported this trend in preterm infants, however found no difference in weight in term infants of either exposure. This trend is more

likely to reflect the impact of early-onset or severe PE, which are associated with greater uteroplacental dysfunction leading to preterm birth.18,66 Compared to previous studies, PE in our

cohort was less severe and less preterm (only 10 (15%) of PE-exposed infants were born before 34 weeks), consistent with the expected rate in an unselected population. Furthermore, earlier

studies did not adjust for preterm birth, SGA or VLBW status, common comorbidities experienced by PE-exposed infants, which are all independently associated with infant postnatal

growth.14,52,53 Our findings support previous literature finding that PE-exposed infants ‘catch up’ to their normotensive counterparts in respect to growth outcomes.67,68 Correspondingly, we

reported that PE-exposed infants experienced greater increases in weight z-score from birth to 2 years, independent of SGA and prematurity status. While FGR and subsequent SGA birth, common

complications of PE, are associated with impaired infant growth,14,52,53 many SGA born neonates experience accelerated weight gain, possibly as a response to intrauterine undernutrition or

clinical intervention where calories are added to feeds. This is referred to as ‘rapid catch-up growth’, an example of how infants born on weight extremes may experience natural regression

to the mean postpartum.44,63 We reported this is our cohort from birth to 6 months,54 as well as in this study from birth to 2 years, irrespective of PE or NTP exposure. However, we also

demonstrated that PE exposure is associated with accelerated infant weight gain, independent of confounders including prematurity and SGA status, which supports an intrauterine programming

effect of PE as suggested by the DOHaD hypothesis. While adjusted confounders may reflect certain shared genetic predispositions and postnatal environmental factors such as infant feeding

practices, we still cannot exclude residual confounding. Although conditional weight gain, which corrects for the regression to the mean that SGA infants may experience, approached

significance from birth to 2 years, it was not different between groups, and thus further differentiation of the impact of SGA status is required in similar cohorts. GH-exposed infants in

our cohort did not differ significantly from NTP infants in weight, and while they experienced greater increases in weight z-score in infancy, this was not independent of perinatal

confounders. This supports the hypothesis that shared lifestyle or genetic risk factors that predispose to both HDP and childhood morbidity, such as an adverse cardiometabolic profile, are

responsible for their increased disease risk rather than an intrauterine programming effect.8,22 This may also explain why GH and late-onset PE, where there is less uteroplacental

dysfunction, are associated with increased risks of childhood morbidity.18,66 Whether a result of GH and PE independently or in combination with these external factors, the increased growth

trajectories and rapid weight gain experienced by exposed infants have nonetheless been associated with greater risks of obesity and cardiometabolic disease in later childhood.46

Furthermore, by age 20, Davis et al.68 described that those exposed to GH and PE causing preterm birth had a three-fold risk of hypertension, and those exposed to GH resulting in term birth

had a two-fold risk of having obesity. Our findings suggest a need in primary care to identify accelerated growth trajectories in infants exposed to HDP and early screening for markers of

cardiometabolic disease.69 Interventions to prevent accelerated weight gain trajectories could include strategies to increase the duration of breastfeeding, which is associated with reduced

risk of future child and maternal cardiometabolic disease.70 In our study both hypertensive groups breastfed for a shorter duration compared to NTP. Furthermore, the introduction of greater

nutrient-rich solid-feeding diets, strategies to combat fussy eating, and the encouragement of greater maternal and infant physical activity may improve future infant health outcomes.54

Strengths of this study include our ethnically diverse cohort, and similar to our previous study,54 our use of the INTERGROWTH-21st Preterm Postnatal Growth Standards,61 which consider the

differing postnatal growth patterns of preterm infants.61 Furthermore, our calculation of conditional weight gain was an additional outcome that considered the potential confounding of age,

sex, birthweight, and regression to the mean on z-score change that SGA infants in our cohort may have experienced.54,63,64 Limitations of this study include the small sample size of GH

infants that reduced statistical power and limited our ability to include further covariates in regression models, and the medium sample of PE infants that prevented sub-analyses based on PE

onset or severity. Although SGA and prematurity status are common complications of PE, in some cases they are unrelated to PE, and adjustment for them in regression may have led to the

overestimation of the impact of PE. We also lacked data on other confounding factors that may influence infant growth, including paternal factors such as height, weight, cardiometabolic

profiles and other genetic or inheritable risk factors, postnatal infant solid feeding practices, activity levels, and the general postnatal environment including infections. Finally, the P4

Study was single-centred, and powered to detect differences in maternal BP outcomes 6 months after NTP, GH or PE exposure rather than paediatric outcomes specifically. GH and PE are common

obstetric complications with known long-term complications for mother and child. We demonstrated that HDP-exposed infants experience accelerated weight gain from birth to 2 years. For

PE-exposed infants, this was independent of commonly comorbid intermediates including SGA and prematurity status, suggesting that PE may have an intrauterine programming effect. However,

further research in larger, term-born, non-SGA cohorts is needed to further disentangle these covariates to understand the specific pathophysiological implications of GH and PE exposure.

Nonetheless, these disorders are commonly comorbid to complications like SGA and prematurity status, and thus our findings provide opportunities for clinical intervention. DATA AVAILABILITY

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PubMed  PubMed Central  Google Scholar  Download references ACKNOWLEDGEMENTS We acknowledge the Bidjigal people of the Eora Nation, and Gweagal people who are the traditional custodians of

the Land on which our research was conducted. We acknowledge the Indigenous women, infants and families who participated in this study, and thank all women and their families for their

ongoing participation in and support for the P4 Study. We also acknowledge the students involved in the collection of data as part of this study as well as paediatricians Prof. Maria Craig,

Dr Ana Dosen, Dr Scott Dunlop, Dr Melanie Fentoulis, Dr Joseph Khouri, Dr Lynette Khoury and Dr Darren Shepherd who were all involved in collecting the paediatric growth measures. FUNDING

Funding for the P4 Study was provided by the St George and Sutherland Medical Research Foundation and a philanthropic donation from Emeritus Professor Richard Henry. Open Access funding

enabled and organized by CAUL and its Member Institutions. AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Discipline of Paediatrics and Child Health, School of Clinical Medicine, UNSW

Medicine and Health, Sydney, NSW, Australia Megan L. Gow, Joseph M. Khouri & Maria E. Craig * Department of Women’s and Children’s Health, St George Hospital, Sydney, NSW, Australia

Megan L. Gow, Lynne Roberts, Greg Davis, Joseph M. Khouri & Amanda Henry * The University of Sydney Children’s Hospital Westmead Clinical School, Sydney, NSW, Australia Megan L. Gow 

& Maria E. Craig * Discipline of Women’s Health, School of Clinical Medicine, UNSW Medicine and Health, Sydney, NSW, Australia Priya Vakil, Greg Davis, Ana Dosen & Amanda Henry * St

George and Sutherland Clinical Campus, School of Clinical Medicine, UNSW Medicine and Health, Sydney, NSW, Australia Lynne Roberts & Mark A. Brown * Renal Medicine, St George Hospital,

Sydney, NSW, Australia Mark A. Brown * Department of Paediatrics, St George Hospital, Sydney, NSW, Australia Maria E. Craig * The George Institute for Global Health, Sydney, NSW, Australia

Amanda Henry Authors * Megan L. Gow View author publications You can also search for this author inPubMed Google Scholar * Priya Vakil View author publications You can also search for this

author inPubMed Google Scholar * Lynne Roberts View author publications You can also search for this author inPubMed Google Scholar * Greg Davis View author publications You can also search

for this author inPubMed Google Scholar * Joseph M. Khouri View author publications You can also search for this author inPubMed Google Scholar * Ana Dosen View author publications You can

also search for this author inPubMed Google Scholar * Mark A. Brown View author publications You can also search for this author inPubMed Google Scholar * Maria E. Craig View author

publications You can also search for this author inPubMed Google Scholar * Amanda Henry View author publications You can also search for this author inPubMed Google Scholar CONTRIBUTIONS

Substantial contributions to conception and design: G.D., M.A.B., M.E.C., A.H. Substantial contributions to acquisition of data: L.R., J.M.K., A.D. Substantial contributions to analysis and

interpretation of data: M.L.G., PV. Drafting the article or revising it critically for important intellectual content: all authors. Final approval of the version to be published: all

authors. CORRESPONDING AUTHOR Correspondence to Megan L. Gow. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no competing interests. CONSENT STATEMENT Written informed consent

for mother and infant was obtained at study enrolment, which occurred by 6 months postpartum. ADDITIONAL INFORMATION PUBLISHER’S NOTE Springer Nature remains neutral with regard to

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2 years after hypertensive versus normotensive pregnancy: a P4 study. _Pediatr Res_ 95, 275–284 (2024). https://doi.org/10.1038/s41390-023-02789-7 Download citation * Received: 07 March

2023 * Revised: 23 July 2023 * Accepted: 09 August 2023 * Published: 06 September 2023 * Issue Date: January 2024 * DOI: https://doi.org/10.1038/s41390-023-02789-7 SHARE THIS ARTICLE Anyone

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