The correlation analysis of weight and blood pressure during the pregnancy and its influencing factors: a retrospective study

Abstract

This study aimed to evaluate the correlation between maternal weight and blood pressure during pregnancy and determine the magnitude of blood pressure changes per kilogram of weight gained. Additionally, we investigated whether this relationship differs among women with gestational diabetes mellitus (GDM) and various categories of hypertensive disorders of pregnancy. This retrospective cohort study analyzed 4,051 pregnancies delivered at Tianjin Medical University Second Hospital between January 2019 and December 2020. We performed covariance analysis controlling for maternal age, gestational weight gain, and neonatal birthweight, followed by simple linear regression to quantify blood pressure changes per kilogram of maternal weight. Subgroup analyses examined these relationships in women with and without GDM, chronic hypertension (CH), gestational hypertension (GH), and normotensive pregnancies. A moderate correlation existed between maternal weight and both systolic (r = 0.427, p < 0.001) and diastolic (r = 0.397, p < 0.001) blood pressure. Each kilogram increase in maternal weight was associated with a 0.47mmHg increase in systolic and 0.325mmHg increase in diastolic blood pressure. These correlations were comparable between women with and without GDM (r = 0.411 vs. r = 0.406 for systolic; r = 0.392 vs. r = 0.372 for diastolic blood pressure). However, correlations were notably attenuated in women with chronic hypertension (r = 0.202 for systolic; r = 0.095 for diastolic blood pressure) compared to those with gestational hypertension or normotensive pregnancies. Maternal weight demonstrates a moderate correlation with blood pressure during pregnancy, with greater impact on systolic than diastolic parameters. This relationship remains consistent regardless of gestational diabetes status but is significantly diminished in women with chronic hypertension. Appropriate weight management may contribute to blood pressure control during pregnancy, particularly for women without pre-existing hypertensive disease.

Introduction

Overweight and obesity represent significant global health challenges that have supplanted malnutrition and starvation as predominant nutritional concerns in many regions worldwide. The contemporary nutritional transition is characterized by increased access to calorie-dense foods alongside increasingly sedentary lifestyles. In China specifically, the popularity of high-calorie beverages such as milky tea exemplifies changing dietary patterns. Concurrently, the psychological stressors associated with educational and professional advancement have fostered maladaptive eating behaviors and contributed to weight management difficulties among modern populations¹. According to a previous report of World Health Organization, approximately one in eight of the global population was affected by obesity, with the concerning statistic that over 390 million children and adolescents were classified as overweight in 2022². Obesity is recognized as a marker of metabolic dysregulation and represents a significant risk factor for numerous pathologies including cardiovascular disease, endocrinopathies, specific malignancies, psychological disorders, sleep disturbances, and skeletal conditions^3–5. The resultant disease burden imposes substantial economic costs on healthcare systems while simultaneously diminishing quality of life for affected individuals⁶. Among obesity-related disorders, hypertension carries particularly significant risks due to its association with potentially fatal complications including cardiac failure and cerebrovascular hemorrhage.

The pathophysiological mechanisms linking adiposity and hypertension are multifaceted. Adipose tissue functions not merely as an energy reservoir but as an active endocrine organ with immunomodulatory properties, involvement in oxidative stress pathways, hemostatic function, and participation in the renin-angiotensin-aldosterone system^7,8. In individuals with obesity, who constitute greater than 40% of the hypertensive population⁹, excessive adipose tissue disrupts the equilibrium of adipocytokines such as adiponectin and leptin. This disruption adversely affects functional vascular tone and smooth muscle cell proliferation through mechanisms involving endothelial nitric oxide synthase. Furthermore, increased adipocyte mass promotes excessive lipolysis, resulting in elevated circulating free fatty acids that contribute to impaired glucose tolerance, endothelial dysfunction, and accelerated atherogenesis. The combined effects of hyperglycemia, pathological sodium and water retention, and increased vascular resistance culminate in the pathophysiological changes as characteristic of essential hypertension^10,11. Consequently, obesity demonstrates a definitive association with hypertension pathogenesis through advanced cardiovascular damage and endocrine dysregulation. Weight management strategies, complemented by appropriate physical activity and diet control, are now recognized as effective interventions for mitigating hypertension-related morbidity¹².

While obesity has been established as a risk factor for hypertensive disorders of pregnancy (HDP), and guidelines recommend appropriate gestational weight gain for prevention, pregnant women experience distinctive physiological adaptations to accommodate fetal development. Moreover, hypertensive disorders of pregnancy demonstrate pathogenetic mechanisms distinct from essential hypertension, particularly with regards to inadequate trophoblastic invasion and placental insufficiency¹³. Gestational weight gain typically follows a continuous trajectory and encompasses not only maternal adipose tissue expansion, but also fetal growth and physiological fluid retention associated with increased circulatory volume¹⁴. Maternal cardiovascular and endocrine adaptations during pregnancy produce characteristic blood pressure patterns, including mid-gestational reductions in blood pressure, while placental dysfunction in hypertensive disorders of pregnancy may precipitate blood pressure elevations prior to 20 weeks’ gestation^15,16. Consequently, the relationship between maternal weight and blood pressure during pregnancy is considerably more complex than in non-pregnant populations and remains incompletely understood.

The HDP represents a leading cause of maternal mortality worldwide and significantly increase the incidence of cesarean delivery and postpartum hemorrhage. Additionally, these disorders are associated with a series of neonatal complications including preterm birth and elevated long-term cardiovascular and metabolic risk¹⁷. Unlike other obstetric complications for which precise diagnostic modalities or effective therapeutic interventions exist, such as echocardiography for congenital cardiac anomalies or ergometrine for postpartum hemorrhage, hypertensive disorders of pregnancy present persistent management challenges. Pre-pregnancy body mass index and abnormal gestational weight gain have been identified as risk factors for both the incidence and progression of hypertensive disorders of pregnancy¹⁸.

Given these associations, there is substantial clinical value in elucidating the specific relationship between maternal weight and blood pressure throughout gestation. This knowledge would enhance understanding of the importance of appropriate weight management for all pregnant women, not exclusively those with established risk factors. Furthermore, considering the pronounced insulin resistance and endothelial dysfunction as characteristics of both gestational diabetes mellitus and hypertensive disorders of pregnancy, investigation of subgroup-specific correlations between weight and blood pressure may identify populations requiring more stringent weight management protocols. Hypertensive disorders of pregnancy present an unavoidable challenge in obstetric practice due to their high prevalence and association with severe maternal complications including cardiac decompensation, placental abruption, and eclampsia. Unfortunately, the pathogenesis and predictive markers of these disorders remain incompletely characterized. Therefore, identification of modifiable risk factors for blood pressure dysregulation during pregnancy has substantial clinical significance. The fertility rate in contemporary society has shown a persistent decline, while obesity prevalence continues to increase, a trend particularly evident in China¹⁹. This demographic shift necessitates heightened attention to maternal safety.

Weight measurement represents a routine, accessible, and relatively objective component of antenatal surveillance, similar to symphysis-fundal height and abdominal circumference assessment. Excessive gestational weight gain may indicate not only pathological fluid retention and hypoalbuminemia—indirect markers of disease progression in hypertensive disorders of pregnancy—but potentially reflects suboptimal self-regulation and lifestyle habits. Additionally, traditional perspectives in Chinese culture place considerable emphasis on fetal well-being, potentially encouraging excessive maternal nutritional intake without adequate consideration of adverse consequences. Considering the established role of obesity in the pathogenesis of both essential hypertension and hypertensive disorders of pregnancy, this study aims to characterize the quantitative relationship between maternal weight and blood pressure during pregnancy, with the goal of emphasizing the importance of appropriate weight management. This retrospective investigation specifically sought to (1) determine the mathematical correlation between maternal weight and both systolic and diastolic blood pressure throughout pregnancy; (2) calculate the magnitude of blood pressure change (in millimeters of mercury) associated with each kilogram of maternal weight gain; (3) investigate whether the weight-blood pressure relationship differs significantly among women with gestational diabetes mellitus compared to those without this condition; and (4) examine whether the correlation between weight and blood pressure varies across hypertensive disorder subgroups, specifically chronic hypertension, gestational hypertension, and normotensive pregnancies.

Through addressing these objectives, this research aims to provide evidence-based guidance for antepartum weight management strategies, potentially improving maternal and perinatal outcomes through enhanced blood pressure control. If significant correlations are identified, particularly in specific high-risk subgroups, more intensive dietary counseling and weight monitoring protocols could be implemented for these populations. Conversely, the absence of strong correlations would suggest that other pathophysiological mechanisms predominate in the development of hypertensive disorders of pregnancy, directing future research toward alternative preventive strategies.

Materials and methods

Study design and ethical approval

This investigation employed a retrospective cohort design examining pregnancies managed and delivered in the obstetric service of Tianjin Medical University Second Hospital from January 2019 through December 2020. The study protocol received approval from the Human Research Ethics Committee of the Tianjin Medical University Second Hospital (approval number: KY2024K068) and was conducted in accordance with all relevant guidelines and regulations. Informed consent was obtained from all participants prior to inclusion in the analysis.

Data sources and collection

Comprehensive maternal and neonatal data were compiled from two complementary institutional databases. Demographic information, prenatal examination records, and serial clinical measurements were extracted from the Tianjin Maternal and Child Health Care Information System (accessed via 60.29.92.68:82/Site/NewTjsfezxSite/Default.aspx). Additional peripartum information, including delivery circumstances and neonatal outcomes, was obtained from the hospital’s In-patient Management Information System. Data extraction was performed by two independent investigators (JL and YW) with discrepancies resolved through consensus discussion with a third reviewer (JR).

Study population

The initial data extraction yielded records from 4,299 pregnant women who received standardized antenatal care and subsequently delivered at our institution during the defined study period. Figure 1 illustrates the participant selection process through a CONSORT-style flow diagram.

Fig. 1.

The flow chart of research.

Inclusion criteria for study participation comprised singleton pregnancy, absence of tobacco or alcohol consumption during pregnancy, and maternal age of 18 years or greater at the time of delivery. Participants were excluded if they had documented pre-existing hyperthyroidism, renal disease, organic cardiac disease, immune system disorders, neurological disease, or chromosomal abnormalities. Additionally, cases with substantial missing antenatal examination data were excluded from analysis. After application of these criteria, 4,051 pregnancies qualified for the final analysis cohort.

Variable definitions and clinical classifications

Classification of hypertensive disorders of pregnancy adhered to the 2021 guidelines published by the International Society for the Study of Hypertension in Pregnancy (ISSHP)²⁰. For analytical purposes, participants were categorized into the following groups: the Normotensive Group, comprising women who maintained blood pressure below 140/90 mmHg throughout pregnancy without antihypertensive medication; the Gestational Hypertension Group (GH), encompassing gestational hypertension, preeclampsia, and eclampsia; and the Chronic Hypertension Group (CH), including chronic hypertension in pregnancy and chronic hypertension with superimposed preeclampsia.

Diagnostic criteria for gestational diabetes mellitus followed the 2019 American Diabetes Association guidelines²¹. For study purposes, diabetes classifications included the Non-diabetic Group (nGDM), consisting of women without evidence of carbohydrate intolerance, and the Diabetic Group (GDM), encompassing both gestational diabetes mellitus and pregestational diabetes mellitus.

All blood pressure measurements were obtained by trained healthcare professionals using calibrated automated oscillometric devices (Omron HBP-1300, Omron Healthcare, Kyoto, Japan) according to standardized institutional protocols. Participants were seated with proper cuff sizing, and measurements were taken after a minimum 5-minute rest period. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded at each antenatal visit, with particular attention to initial (basic) blood pressure obtained at first antenatal appointment, serial blood pressure documented at each trimester during standardized prenatal visits, admission blood pressure recorded upon hospital admission for delivery, and delivery blood pressure measured during the intrapartum period.

Maternal weight was measured using calibrated electronic scales (Seca 763, Seca GmbH, Hamburg, Germany) with participants in light clothing and without footwear. Height was measured using a wall-mounted stadiometer. Body Mass Index (BMI) was calculated as weight in kilograms divided by height squared in meters at initial presentation. Gestational weight gain (GWG) was determined as the difference between final documented weight prior to delivery and pre-pregnancy weight. Serial weight measurements were obtained at each standard antenatal visit throughout gestation.

Statistic analysis

With the help of SPSS software version 29.0 (IBM Corporation, Armonk, NY, USA) and Prism version 10 (GraphPad Software, San Diego, CA, USA), Our statistical analyses were performed. Continuous variables with normal distribution were presented as mean ± standard deviation, while non-normally distributed variables were expressed as median with interquartile range. Categorical variables were presented as frequencies and percentages. Between-group comparisons for normally distributed continuous variables employed independent samples t-tests, while categorical variables were compared using chi-square tests. Statistical significance was defined as p < 0.05 for all analyses. The relationship between maternal weight and blood pressure was evaluated through multiple analytical approaches. Covariance analysis was performed to identify correlations between weight and blood pressure while controlling for potential confounding variables including maternal age, gestational weight gain, and neonatal birthweight. Multiple linear regression models were constructed to determine factors significantly associated with systolic and diastolic blood pressure at hospital admission. Independent variables included maternal age, educational attainment, parity, gestational weight gain, pre-pregnancy BMI, hypertensive disorder diagnosis, gestational diabetes diagnosis, delivery method, maternal weight at admission, gestational age at admission, and gestational age at delivery. Collinearity was assessed using variance inflation factor (VIF) analysis with values exceeding 10 indicating significant multicollinearity. Pearson correlation analysis was applied to determine the strength of association between maternal weight and blood pressure measurements. Correlation coefficients were interpreted as follows: 0.80-1.00 (very strong), 0.60–0.79 (strong), 0.40–0.59 (moderate), 0.20–0.39 (weak) and 0.00-0.19 (very weak). Simple linear regression was utilized to quantify the magnitude of blood pressure change associated with each kilogram increase in maternal weight. Separate equations were derived for systolic and diastolic blood pressure in the entire cohort and within predefined clinical subgroups. The coefficient of determination (R²) was calculated to assess the proportion of blood pressure variance explained by maternal weight.

Results

Participant characteristics

The final analysis cohort comprised 4,051 pregnancies, of which 2,796 (69.02%) were normotensive and 1,255 (30.98%) were classified as having hypertensive disorders of pregnancy (HDP). Table 1 presents the demographic and clinical characteristics of these groups. The mean maternal age was comparable between normotensive (30.21 ± 4.41 years) and hypertensive (30.30 ± 4.16 years) women (p = 0.26). Significant differences were observed in pre-pregnancy body mass index, with the HDP group demonstrating higher values (25.24 ± 4.66 kg/m²) compared to the normotensive group (22.29 ± 3.27 kg/m²; p < 0.001). The proportion of primiparous women was significantly higher in the HDP group (68.37%) compared to the normotensive group (58.08%; p < 0.001). Educational attainment differed significantly between groups, with 78.54% of normotensive women and 74.18% of women with HDP having undergraduate or graduate education (p < 0.002).

Table 1.

The demographic and clinical characteristics of the normal and HDP group.

	Normal group n = 2796	HDP group n = 1255	t/z value	P value
Delivery age, years	30.21 ± 4.41	30.30 ± 4.16	−0.63	0.26
Basic BMI, kg/m*2	22.29 ± 3.27	25.24 ± 4.66	−20.31	<0.001
GWG, kg	13.35 ± 4.56	13.60 ± 5.62	−1.40	0.08
Primipara, n	1624(58.08%)	858(68.37%)	38.60	<0.001
Undergraduate& graduate, n	2196(78.54%)	931(74.18%)	9.342	<0.002
Basic SBP, mmHg	107.3 ± 10.41	116.56 ± 12.60	−22.77	<0.001
Basic DBP, mmHg	69.45 ± 7.43	76.22 ± 9.31	−22.72	<0.001
Admission time, weeks	38.81 ± 1.75	38.41 ± 2.15	5.75	<0.001
Admission SBP, mmHg	119.46 ± 9.91	137.16 ± 14.70	−37.87	<0.001
Admission DBP, mmHg	78.68 ± 7.61	92.19 ± 10.23	−41.87	<0.001
Delivery time, weeks	38.94 ± 1.76	38.57 ± 2.12	5.35	<0.001
Delivery SBP, mmHg	116.21 ± 9.13	126.70 ± 13.35	−25.30	<0.001
Delivery DBP, mmHg	78.68 ± 7.61	79.19 ± 10.35	−1.56	0.06
Apgar score(1 min), n	9.281 ± 0.10	9.05 ± 1.34	5.55	<0.001
Apgar score(5 min), n	9.87 ± 0.53	9.73 ± 0.84	5.50	<0.001
Apgar score(10 min), n	9.97 ± 0.32	9.92 ± 0.63	2.58	0.01
Newborn weight, g	3263.30 ± 477.75	3201.38 ± 655.73	3.01	0.001
Newborn length, cm	49.71 ± 1.49	49.38 ± 2.42	4.42	<0.001
Caesarean section, n	1299(46.46%)	769(61.27%)	76.09	<0.001
GDM, n	685(24.50%)	479(38.17%)	79.02	<0.001

Initial blood pressure parameters at first antenatal visit were significantly elevated in the HDP group, with systolic blood pressure of 116.56 ± 12.60 mmHg versus 107.3 ± 10.41 mmHg in normotensive women (p < 0.001), and diastolic blood pressure of 76.22 ± 9.31 mmHg versus 69.45 ± 7.43 mmHg in normotensive women (p < 0.001). This pattern persisted at hospital admission, with higher systolic (137.16 ± 14.70 versus 119.46 ± 9.91 mmHg; p < 0.001) and diastolic (92.19 ± 10.23 versus 78.68 ± 7.61 mmHg; p < 0.001) blood pressure in the HDP group. Gestational age at both admission and delivery was significantly lower in the HDP group (p < 0.001 for both comparisons).

Neonatal outcomes demonstrated significant differences between groups. Apgar scores at 1, 5, and 10 min were consistently lower in the HDP group (p < 0.001, p < 0.001, and p = 0.01, respectively). Newborn weight (3201.38 ± 655.73 versus 3263.30 ± 477.75 g; p = 0.001) and length (49.38 ± 2.42 versus 49.71 ± 1.49 cm; p < 0.001) were significantly reduced in infants born to mothers with HDP. The cesarean delivery rate was substantially higher in the HDP group (61.27%) compared to the normotensive group (46.46%; p < 0.001). Gestational diabetes mellitus was significantly more prevalent among women with HDP (38.17%) compared to normotensive women (24.50%; p < 0.001).

Notably, despite the higher pre-pregnancy BMI in the HDP group, gestational weight gain did not differ significantly between hypertensive (13.60 ± 5.62 kg) and normotensive (13.35 ± 4.56 kg) pregnancies (p = 0.08). Similarly, no significant difference was observed in diastolic blood pressure at delivery between the groups (p = 0.06).

Factors influencing blood pressure at hospital admission

Multiple linear regression analysis identified several significant predictors of systolic blood pressure at admission (Table 2). Nulliparity was associated with reduced systolic blood pressure (β = -0.86 mmHg, p = 0.041), while gestational weight gain demonstrated a positive association (β = 0.145 mmHg per kilogram, p = 0.023). As expected, the diagnosis of hypertensive disorders of pregnancy exerted the strongest influence, with a substantial negative standardized coefficient (β = -15.735, p < 0.001). Gestational diabetes mellitus was associated with reduced systolic blood pressure (β = -1.048 mmHg, p = 0.011), and cesarean delivery pattern showed a positive association (β = 1.075 mmHg, p = 0.004). Other variables, including maternal age, educational attainment, pre-pregnancy BMI, admission weight, admission gestational age, and delivery gestational age did not demonstrate significant associations with systolic blood pressure at admission.

Table 2.

The multiple linear regression for the influence factors of SBP at admission.

	Unstandardized coefficient		Standardized coefficient	t	Sig	Collinearity Statistics VIF
	B	Standard error
(Constant)	189.605	4.433		42.768	<0.001
Delivery Age	0.026	0.048	0.008	0.55	0.582	1.338
Education	−0.698	0.446	−0.021	−1.564	0.118	1.125
Nulliparous	−0.86	0.421	−0.03	−2.04	0.041	1.356
GWG	0.145	0.064	0.05	2.274	0.023	3.163
Basic BMI	0.217	0.136	0.061	1.594	0.111	9.486
HDP	−15.735	0.415	−0.512	−37.884	<0.001	1.186
GDM	−1.048	0.415	−0.033	−2.529	0.011	1.133
Delivery pattern	1.075	0.377	0.038	2.855	0.004	1.139
Admission weight	0.082	0.046	0.069	1.785	0.074	9.562
Admission time	0.09	0.841	0.012	0.107	0.914	81.196
Delivery time	−1.362	0.84	−0.181	−1.621	0.105	81.093

Analysis of factors influencing diastolic blood pressure at admission revealed a somewhat different pattern (Table 3). Nulliparity again showed a negative association (β = -0.876 mmHg, p = 0.005), while pre-pregnancy BMI demonstrated a positive relationship (β = 0.205 mmHg per kg/m², p = 0.043). The diagnosis of hypertensive disorders of pregnancy remained the strongest predictor (β = -12.276, p < 0.001), and gestational diabetes mellitus was associated with reduced diastolic blood pressure (β = -0.69 mmHg, p = 0.025). Unlike for systolic blood pressure, delivery pattern did not significantly influence diastolic blood pressure at admission, nor did gestational weight gain.

Table 3.

The multiple linear regression for the influence factors of DBP at admission.

	Unstandardized coefficient		Standardized coefficient	t	Sig	Collinearity Statistics VIF
	B	Standard error
(Constant)	121.419	3.299		36.806	< 0.001
Delivery Age	0.038	0.036	0.015	1.068	0.286	1.338
Education	−0.581	0.332	−0.023	−1.75	0.08	1.125
Nulliparous	−0.876	0.314	−0.04	−2.793	0.005	1.356
GWG	0.049	0.048	0.023	1.027	0.305	3.163
Basic BMI	0.205	0.101	0.078	2.024	0.043	9.486
HDP	−12.276	0.309	−0.538	−39.721	< 0.001	1.186
GDM	−0.69	0.309	−0.03	−2.238	0.025	1.133
Delivery pattern	0.281	0.28	0.013	1.004	0.315	1.139
Admission weight	0.027	0.034	0.03	0.784	0.433	9.562
Admission time	0.175	0.626	0.031	0.28	0.779	81.196
Delivery time	−0.776	0.625	−0.139	−1.242	0.214	81.093

Relationship between maternal weight and blood pressure throughout pregnancy

Covariance analysis controlling for maternal age, gestational weight gain, and neonatal birthweight revealed a significant but weak correlation between maternal weight and both systolic (r = 0.322, p < 0.001) and diastolic (r = 0.304, p < 0.001) blood pressure at hospital admission (Table 4).

Table 4.

The covariance analysis of weight and blood pressure at admission.

Control variable			Weight	SBP	DBP
Delivery age, newborn weight &GWG	weight,	correlation	1.000	0.322	0.304
		Sig(two-tailed test)		< 0.001	< 0.001

Longitudinal assessment of weight and blood pressure patterns throughout gestation demonstrated distinct trajectories. Maternal weight increased progressively throughout pregnancy in a relatively linear pattern (Fig. 2). In contrast, blood pressure exhibited the characteristic mid-pregnancy decline followed by late-gestational increase described in previous literature (Fig. 3).

Fig. 2.

The variation of weight during the pregnancy.

Fig. 3.

The variation of blood pressure during the pregnancy.

Correlation analysis incorporating all antenatal measurements revealed a moderate positive association between maternal weight and systolic blood pressure (r = 0.427, p < 0.001) and a slightly weaker correlation with diastolic blood pressure (r = 0.397, p < 0.001) (Fig. 4). Simple linear regression quantified the magnitude of these relationships, indicating that for each kilogram increase in maternal weight, systolic blood pressure increased by 0.47 mmHg (95% CI: 0.418–0.437; p < 0.001) and diastolic blood pressure increased by 0.325 mmHg (95% CI: 0.387–0.408; p < 0.001). The coefficients of determination (R²) were 0.183 for systolic and 0.158 for diastolic blood pressure, indicating that maternal weight explained approximately 18.3% and 15.8% of the variability in these parameters, respectively (Table 5).

Fig. 4.

The correlation between the weight and blood pressure in pregnancy.

Table 5.

The correlational analysis& simple linear regression of weight and blood pressure during the pregnancy.

	r	Sig	95% CI	Equation of linear regression	Sig	R2
SBP in the pregnancies	0.427	< 0.001	0.418−0.437	Y = 80.987 + 0.47X	< 0.001	0.183
DBP in the pregnancies	0.397	< 0.001	0.387−0.408	Y = 50.296 + 0.325X	< 0.001	0.158
SBP in GDM	0.411	< 0.001	0.392−0.43	Y = 84.629 + 0.441X	< 0.001	0.169
SBP in nGDM	0.406	< 0.001	0.394−0.418	Y = 81.119 + 0.458X	< 0.001	0.165
DBP in GDM	0.392	< 0.001	0.373−0.411	Y = 52.025 + 0.315X	< 0.001	0.154
DBP in nGDM	0.372	< 0.001	0.36−0.385	Y = 50.68 + 0.313X	< 0.001	0.139
SBP in CH	0.202	< 0.001	0.141−0.261	Y = 118.216 + 0.198X	<0.001	0.041
SBP in GH	0.334	< 0.001	0.313−0.354	Y = 93.918 + 0.339X	< 0.001	0.111
SBP in Normal	0.337	< 0.001	0.324−0.35	Y = 85.496 + 0.365X	< 0.001	0.114
DBP in CH	0.095	0.003	0.033−0.157	Y = 82.024 + 0.073X	0.003	0.009
DBP in GH	0.319	< 0.001	0.298−0.339	Y = 58.688 + 0.245X	< 0.001	0.102
DBP in Normal	0.301	< 0.001	0.288−0.314	Y = 54.035 + 0.024X	< 0.001	0.091

Subgroup analysis by gestational diabetes status

Comparison of the weight-blood pressure relationship between women with and without gestational diabetes mellitus revealed comparable correlations. In the GDM group, the correlation coefficient for maternal weight and systolic blood pressure was r = 0.411 (p < 0.001), while in women without GDM, this value was r = 0.406 (p < 0.001) (Fig. 5). Similarly, the correlation between maternal weight and diastolic blood pressure was r = 0.392 (p < 0.001) in women with GDM and r = 0.372 (p < 0.001) in those without GDM (Fig. 6).

Fig. 5.

The comparison of the GDM and nGDM group about the correlation between the weight and SBP.

Fig. 6.

The comparison of the GDM and nGDM group about the correlation between the weight and DBP.

Linear regression analysis quantified these relationships, demonstrating that in women with GDM, each kilogram increase in maternal weight was associated with a 0.441 mmHg increase in systolic blood pressure (95% CI: 0.392–0.43; p < 0.001) and a 0.315 mmHg increase in diastolic blood pressure (95% CI: 0.373–0.411; p < 0.001). In women without GDM, the corresponding values were 0.458 mmHg (95% CI: 0.394–0.418; p < 0.001) for systolic and 0.313 mmHg (95% CI: 0.36–0.385; p < 0.001) for diastolic blood pressure. The coefficients of determination were comparable between groups (Table 5).

Subgroup analysis by hypertension classification

Analysis of the weight-blood pressure relationship across hypertension categories revealed substantial heterogeneity. In women with chronic hypertension, the correlation between maternal weight and systolic blood pressure was weak (r = 0.202, p < 0.001), and the relationship with diastolic blood pressure was negligible (r = 0.095, p = 0.003) (Figs. 7 and 8). In contrast, women with gestational hypertension demonstrated a weak correlation between weight and both systolic (r = 0.334, p < 0.001) and diastolic (r = 0.319, p < 0.001) blood pressure. Normotensive women showed similar correlations (r = 0.337 for systolic and r = 0.301 for diastolic blood pressure, p < 0.001 for both).

Fig. 7.

The comparison of the normotensive, GH, CH group about the correlation between the weight and SBP.

Fig. 8.

The comparison of the normotensive, GH, CH group about the correlation between the weight and DBP.

Quantification of these relationships through linear regression revealed that in women with chronic hypertension, each kilogram increase in maternal weight was associated with a 0.198 mmHg increase in systolic blood pressure (95% CI: 0.141–0.261; p < 0.001) and a 0.073 mmHg increase in diastolic blood pressure (95% CI: 0.033–0.157; p = 0.003). The coefficients of determination were notably low (R² = 0.041 for systolic and R² = 0.009 for diastolic blood pressure), indicating that maternal weight explained only 4.1% and 0.9% of blood pressure variability in this subgroup.

In women with gestational hypertension, each kilogram increase in maternal weight corresponded to a 0.339 mmHg increase in systolic blood pressure (95% CI: 0.313–0.354; p < 0.001) and a 0.245 mmHg increase in diastolic blood pressure (95% CI: 0.298–0.339; p < 0.001). In normotensive women, the values were 0.365 mmHg (95% CI: 0.324–0.35; p < 0.001) for systolic and 0.024 mmHg (95% CI: 0.288–0.314; p < 0.001) for diastolic blood pressure. The coefficients of determination ranged from 0.091 to 0.114, indicating that maternal weight explained approximately 9–11% of blood pressure variability in these subgroups (Table 5).

Discussion

The demographic landscape in contemporary society presents a concerning paradox: declining fertility rates juxtaposed against rising obesity prevalence. This contradiction is particularly pronounced in China, as noted by Chen¹⁹, necessitating heightened vigilance regarding maternal safety during pregnancy. The HDP represents an unavoidable challenge in obstetric practice, ranking among the most common complications and potentially culminating in life-threatening sequelae including cardiac failure, placental abruption, and eclampsia. Despite their clinical significance, the pathophysiological mechanisms and predictive indicators of these disorders remain incompletely elucidated, underscoring the importance of identifying modifiable factors influencing blood pressure regulation during gestation.

Weight assessment constitutes a routine and relatively objective component of antenatal surveillance, comparable to fundal height and abdominal circumference measurements but with reduced vulnerability to observer bias. Excessive gestational weight gain may signify not only pathological fluid retention and hypoalbuminemia—indirect markers of disease progression in hypertensive disorders—but potentially reflects suboptimal dietary discipline and health behaviors. Additionally, cultural factors influence maternal nutrition, particularly in Chinese society where traditional perspectives emphasize fetal well-being, potentially encouraging excessive maternal nutritional intake without adequate consideration of potential adverse maternal consequences. Given the established role of obesity in the pathogenesis of both essential hypertension and pregnancy-specific hypertensive disorders, our investigation sought to characterize the quantitative relationship between maternal weight and blood pressure during pregnancy, with the goal of emphasizing the importance of appropriate weight management.

Tianjin, a coastal metropolis in northern China, is characterized by dietary patterns high in carbohydrates and sodium, predisposing the population to obesity-related conditions. As a regional referral center for high-risk pregnancies, our institution manages substantial numbers of women with hypertensive disorders of pregnancy (30.98%, n = 1,255/4,051) and gestational diabetes mellitus (28.73%, n = 1,164/4,051), providing a robust cohort for investigating these relationships. Our data revealed that 34.90% of women were overweight or obese at their initial antenatal visit, reflecting the concerning prevalence of elevated body mass index in our obstetric population.

The mean gestational weight gain in our cohort was 13.54 kg, with no significant difference observed between normotensive women and those with hypertensive disorders (13.35 kg versus 13.60 kg, p = 0.08). This finding suggests generally appropriate weight management across both groups, likely attributable to consistent antenatal counseling and patient adherence to recommended guidelines. In examining the longitudinal patterns of weight and blood pressure throughout pregnancy, we observed persistent weight gain from conception through delivery, consistent with the expected positive nitrogen balance of gestation (Fig. 2). In contrast, blood pressure demonstrated the characteristic mid-pregnancy nadir (Fig. 3) previously documented in our research¹⁵. This divergence in trajectories suggests that while weight contributes to blood pressure regulation during pregnancy, additional physiological mechanisms substantially influence hemodynamic parameters.

To elucidate the relationship between maternal weight and blood pressure while accounting for potential confounding factors including maternal age, gestational weight gain, and neonatal birthweight¹⁸, we performed covariance analysis. This revealed a significant but modest correlation between maternal weight and both systolic (r = 0.322, p < 0.05) and diastolic (r = 0.304, p < 0.05) blood pressure at hospital admission (Table 4). Comprehensive analysis incorporating all antenatal measurements demonstrated a moderate correlation between maternal weight and blood pressure parameters (r = 0.427 for systolic and r = 0.397 for diastolic blood pressure, p < 0.05). Linear regression quantified these relationships, indicating that each kilogram increase in maternal weight corresponded to elevations of 0.47 mmHg in systolic and 0.325 mmHg in diastolic blood pressure (Fig. 4; Table 5).

Several pathophysiological mechanisms may explain these observed correlations. First, gestational weight gain can induce excessive insulin secretion and insulin resistance. The resulting hyperinsulinemia may enhance renal sodium reabsorption and stimulate the sympathetic nervous system, contributing to blood pressure elevation²². Second, increased adipose tissue, particularly visceral deposits, secretes diverse functional adipocytokines including non-esterified fatty acids, leptin, angiotensinogen, endothelin, interleukin-6, and renin²³. These bioactive molecules collectively influence blood pressure regulation by enhancing α1-adrenoreceptor vasoreactivity while simultaneously reducing baroreflex sensitivity, vascular compliance, and endothelium-dependent vasodilation²⁴.

Additionally, gestational weight gain is frequently accompanied by dyslipidemia, which may exacerbate inflammatory processes and endothelial dysfunction. These pathophysiological alterations potentially contribute to preeclampsia-like phenomena and subsequent blood pressure elevation^25,26. It is noteworthy that obesity directly impacts myocardial contractility and diastolic function, increasing cardiac workload and potentially exacerbating existing hypertensive conditions. The more pronounced effect observed for systolic compared to diastolic blood pressure (0.47 mmHg versus 0.325 mmHg per kilogram) likely reflects the greater impact of these mechanisms on cardiac output rather than peripheral vascular resistance²⁷.

These findings suggest that appropriate weight management may contribute meaningfully to blood pressure control during pregnancy. Conversely, maintaining blood pressure within recommended ranges may help mitigate pathological fluid retention and albumin loss associated with excessive gestational weight gain²⁸. The bidirectional nature of this relationship merits consideration in clinical management protocols for pregnant women, particularly those at elevated risk for hypertensive complications.

Based on the established pathophysiology of obesity, we hypothesized that women with gestational diabetes mellitus and hypertensive disorders would demonstrate stronger correlations between weight and blood pressure due to their pronounced insulin resistance and endothelial dysfunction. Surprisingly, our results revealed no significant difference in this relationship between women with and without gestational diabetes mellitus (Figs. 5 and 6; Table 5). This unexpected finding may reflect the more intensive dietary counseling and weight management typically provided to women with gestational diabetes, potentially mitigating the adverse hemodynamic effects of excessive weight gain.

Perhaps the most notable finding from our subgroup analysis was the markedly attenuated correlation between maternal weight and blood pressure in women with chronic hypertension. In this population, maternal weight demonstrated only a weak correlation with systolic blood pressure (r = 0.202) and virtually no relationship with diastolic blood pressure (r = 0.095) (Figs. 7 and 8; Table 5). This distinct pattern likely reflects the fundamentally different pathophysiology of chronic hypertension compared to gestational forms, particularly regarding reduced vascular elasticity and diminished responsiveness to adipocytokines²⁹. Women with longstanding hypertension typically exhibit structural vascular changes and altered baroreceptor sensitivity that may render blood pressure regulation less dependent on fluctuations in maternal weight.

Our analysis further revealed that correlations between weight and blood pressure in women with gestational hypertension and normotensive pregnancies were comparable. This observation may be attributable to appropriate gestational weight gain across our cohort, as well as the potential mitigating effects of antihypertensive and vasodilatory therapies in women with gestational hypertension. These therapeutic interventions may attenuate blood pressure fluctuations and potentially obscure the influence of maternal weight on hemodynamic parameters.

Our investigation has several limitations that warrant acknowledgment. First, our pregnant test materials lacked comprehensive third-trimester data, as this information was recorded in patient-held pregnancy handbooks rather than institutional electronic databases. This data gap potentially limits our understanding of weight-blood pressure relationships during the critical final weeks of gestation. Second, while our analysis identified significant correlations between maternal weight and blood pressure, the modest coefficients of determination indicate that weight represents just one of many factors influencing blood pressure during pregnancy. The multifactorial nature of blood pressure regulation is reflected in the relatively low R² values, suggesting that comprehensive blood pressure management requires consideration of multiple physiological and environmental factors beyond weight alone.

Future investigations should incorporate additional hemodynamic parameters, including cardiac output, systemic vascular resistance, and biomarkers of endothelial function, to develop more comprehensive models of blood pressure regulation during pregnancy. Prospective studies with standardized measurement protocols and detailed assessment of dietary patterns, physical activity levels, and psychological stressors would further elucidate the complex interplay between maternal weight and blood pressure during gestation. The integration of advanced techniques for body composition analysis, including assessment of visceral adiposity, might provide more nuanced insights regarding the specific adipose depots most strongly associated with adverse hemodynamic effects.

Despite these limitations, our findings have meaningful clinical implications. The quantifiable relationship between maternal weight and blood pressure suggests that appropriate weight management represents a modifiable factor in the prevention and management of hypertensive disorders of pregnancy. The observed differences across hypertensive subgroups indicate that weight management strategies may be particularly beneficial for women with gestational forms of hypertension rather than those with chronic disease.

Conclusions

This investigation demonstrates a moderate correlation between maternal weight and blood pressure during pregnancy, with quantifiable increases in both systolic and diastolic parameters for each kilogram of maternal weight. This relationship appears consistent regardless of gestational diabetes status but varies significantly across hypertensive disorder classifications, with notably diminished correlations in women with chronic hypertension. These findings suggest that appropriate weight management contributes to blood pressure control during pregnancy, particularly for systolic parameters and in women without pre-existing hypertensive disease. Similarly, optimal blood pressure regulation may mitigate pathological fluid retention and disease progression in women with hypertensive disorders of pregnancy, alleviating albumin loss and reducing the risk of adverse maternal and fetal outcomes. The clinical implication of these findings is that weight control is helpful for improving blood pressure during pregnancy, especially for systolic blood pressure, with the exception of patients with chronic hypertension. For patients with hypertensive disorders of pregnancy, appropriate blood pressure regulation may help alleviate pathological fluid retention and mitigate disease progression.

Author contributions

Jie Ren: Project development, Data Collection, Manuscript writing, Jing Li: Data Collection, Zhuoran Fan: Data analysis, Caiyun Zhao: Manuscript Editing, Yujie Wang: Data Collection, Shaofang Hua: Project development.All authors reviewed the manuscript.

Funding

Financial support for this research was provided by the Tianjin Medical University Second Hospital Youth Foundation (grant number: 2023ydey05) and the Natural Science Funds of Tianjin Education Commission (grant number: 2020KJ171).

Data availability

All the data of our study have been recorded in the Scientific Research Section of Tianjin Medical University the Second Hospital and can be acquired by contacting the corresponding author.

Declarations

Competing interests

The authors declare no competing interests.

Ethics approval

This study was approved by the Human Research Ethics Committee of the Tianjin Medical University Second Hospital (approval number: KY2024K068).