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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
REVIEW ARTICLE  
Year : 2019  |  Volume : 30  |  Issue : 2  |  Page : 299-308
Birth weight, gestational age, and blood pressure: Early life management strategy and population health perspective


1 Department of Renal Medicine, The Royal Hospital, Muscat, Oman
2 The Saudi Center for Organ Transplantation, Riyadh, Saudi Arabia
3 Department of Medicine, Ministry of Health and Prevention, Dubai, UAE

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Date of Submission07-Sep-2018
Date of Acceptance10-Oct-2018
Date of Web Publication23-Apr-2019
 

   Abstract 


The incidence of hypertension (HTN) is rising worldwide with an estimated prevalence of 22%, 7.5 million deaths (12.8%). It is a major risk factor for coronary heart diseases and hemorrhagic strokes. In Oman, the crude prevalence of HTN was 33.1%, whereas the age-adjusted prevalence was 38.3%. Among Gulf Cooperation Countries, 47.2% of the individuals were hypertensive, and women were more likely to have HTN than men. Similarly, the prevalence of low-birth-weight (LBW) is also rising globally with the more prevalent incidence in developing countries reaching almost a rate just lower than 20.0/100 births. In Oman, the prevalence of LBW was 4.2% in 1980, which doubled (8.1%) in 2000 and has shown a slow but steady increase reaching 10.2% in 2013. LBW term is the most commonly used surrogate measure of intrauterine growth retardation and has been related to increased cardiovascular mortality, due to increased risk of cardiovascular risk factors, including blood pressure (BP), diabetes, cholesterol level, and other risk factors. The epidemiologic evidence clearly points to an inverse association between birth weight and many hemodynamic cardiovascular risk markers. Possible mechanisms operating in fetal life that might determine BP include the structural development of resistance arteries, the setting of hormone levels, and nephron endowment. Retarded fetal growth leads to permanently reduced cell numbers in the kidney. Patients with high BP had almost 50% less number of glomeruli compared to that of the normotensive individuals, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass. It is not merely a reduced nephron number that is responsible for HTN, but compensatory maladaptive changes that occur internally when nephrogenesis is compromised. The likelihood of an adverse outcome is greatly amplified in those born with LBW who later develop obesity or an increased ponderal index.

How to cite this article:
Al Salmi I, M. Shaheen FA, Hannawi S. Birth weight, gestational age, and blood pressure: Early life management strategy and population health perspective. Saudi J Kidney Dis Transpl 2019;30:299-308

How to cite this URL:
Al Salmi I, M. Shaheen FA, Hannawi S. Birth weight, gestational age, and blood pressure: Early life management strategy and population health perspective. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2019 Jul 17];30:299-308. Available from: http://www.sjkdt.org/text.asp?2019/30/2/299/256836



   Introduction Top


Hypertension (HTN) continues to be one of the main risk factors for cardiovascular disease (CVD) worldwide. It is a leading risk factor for morbidity and mortality in the world. The reported prevalence of HTN varies worldwide, with the lowest prevalence in rural India (3.4% in men and 6.8% in women) and the highest prevalence in Poland (68.9% in men and 72.5% in women).[1] Approximately 75 million adults have been diagnosed with HTN in the United States, and among Industrialized countries, it affects 25%–35% of individuals globally. HTN is estimated to cause 4.5% of the current global disease burden and is prevalent in many developing countries as in the developed world.[1]

In Oman, the age-adjusted prevalence of the metabolic syndrome was 21.0%, and over 87% of Omanis had at least one CVD risk factor (38% had hyperglycemia, 19% HTN and 34.5% had high total cholesterol).[2],[3] In Gulf Cooperation Countries (GCC) which consists of six countries, Bahrain, Kuwait, Oman, Qatar, Saudi Arabia, and United Arab Emirates (UAE), HTN ranged from 20.9 to 53%.[4],[5] The prevalence of HTN was also high among women in GCC countries. Data from the Second Gulf Registry of Acute Coronary Events (GulfRACE-2) showed that 47.2% of the registered individuals were hypertensive, and women were more likely to have HTN than men. It is forecasted that the number of people affected by HTN will endure a very high upsurge and, by 2025, approximately 1.5 billion individuals will be affected.[6]

Birth weight varies globally. The highest proportion of low-birth-weight (LBW) babies in the world are born in Indian sub-continent where LBW babies are born at rate just lower than 20.0/100 births.[7] In Oman, LBW was 10.2% out of a total live birth of over 66,000 live birth during 2013. The worldwide prevalence of LBW is 15.5%, which amounts to about 20 million LBW infants born each year, 96.5% of them in the developing countries.[7] LBW has been increasing globally and regionally with various advancement in medical care; including that of obstetric and neonatal care and technological development with restricted growth, and pregnancy complications are taking place as live births. For example, in Oman, the prevalence of LBW was 4.2% in 1980, which doubled (8.1%) in 2000 and has shown a slow but steady increase reaching 10.2% in 2013.[8] This also causes an increase in the rate of LBW infants, and subsequently an increased rate of long-term medical sequelae.

Recently, over the last few decades, much attention has been steered toward the contribution of the intrauterine environment to the development of chronic and noncommunicable diseases (NCD). Epidemiological studies have demonstrated that a poor intrauterine environment is associated with an increased risk of HTN, chronic kidney disease, and diabetes.[7],[8],[9] Barker and Martyn hypothesized that nutrient deprivation during distinct periods of organ development prenatally programs the offspring for CVD later in life.[7],[8] It is now well proven that LBW, reflecting a poor intrauterine environment,[10] is associated with diminished nephron endowment and other pathophysiological mechanisms predisposing to the development of high blood pressure (BP).[11],[12]


   Epidemiological Evidence of the Relationship between Birth Weight and Blood Pressure Top


Essential HTN is multi-factorial in the cause, with both genetic and environmental components.[10] Several epidemiological studies have reported that LBW is associated with increased BP throughout various stages of life including infancy,[13] childhood,[11],[12],[13] childhood-adult,[14],[15],[16],[17] and adult life.[18],[19],[20] However, this relationship also has an important relation to catch up growth.[21],[22],[23]

A systematic review of 34 studies, based on >66,000 people, found that in both adults and prepubertal children, there was a consistent negative relationship between birth weight and current BP.[24] Another systemic review of more than 80 studies confirmed the inverse relationship between birth weight and BP.[25] However, others had criticized the claims of a strong inverse association between birth weight and subsequent BP may chiefly reflect the impact of random error, selective emphasis of particular results, and inappropriate adjustment for current weight and for confounding factors. Their systemic review findings suggest that birth weight is of little relevance to BP levels in later life.[10] The magnitude of the birth weight–BP association was found to increase with increasing age from childhood to adulthood.

Huxley et al review of 45 pediatric and adult studies reported a negative relationship between birth weight and systolic BP. They reported that for each one-kilogram increase in birth weight was associated with an almost 2 mm Hg/kg decrease in systolic BP.[10],[23] Other reviews of adult studies also were consistent with the earlier ones which showed a similar consistent negative association between birth weight and BP.[21],[22] Of the 28 cohort studies, 25 studies found an inverse association; however, not all were adjusted for body mass index (BMI). More recently, a meta-analysis of 27 studies conducted between 1995 and 2012 found that LBW (<2500 g) compared with birth weight greater than 2500 g was associated with an increased risk of HTN (odds ratio 1.21; 95% confidence interval 1.13, 1.30).[24],[25] Al Salmi et al took advantage of the longitudinal population-based resources of the AusDiab study (the Australian Diabetes, Obesity, and Lifestyle study), which is the national Australian longitudinal population-based study, to examine the prevalence and incidence of diabetes and its complications, to examine the associations of birth weight and BP in the general adult population of Australia.[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42],[43] It is the first study of its kind to examine the effect of birth weight on the development of multiple of chronic diseases in a representative adult population. A significant association was identified between birth weight and systolic BP, diastolic BP, and HTN. This applied in analyses of unadjusted data in females and significance relationship persisted with adjustment for the age and current body size for both females and males. Furthermore, the relationship persisted with adjustment for physical activity, smoking, alcohol intake, family history, and current socioeconomic status.[31],[32],[33],[34]

Amplification of birth weight effect

The likelihood of an adverse outcome is greatly amplified in those born with LBW, who later develop obesity or an increased ponderal index (weight × 100]/(length3). Conversely, those born with LBW, who continue to be small or thin, are relatively protected in terms of metabolic demand in adult life.[28] Hence, researchers found that the rise of BP with age is closely related to growth and is accelerated by the adolescent growth spurt.[19],[44] An interaction between prenatal exposure and postnatal dietary intake may determine the level of HTN.[45] A study of children concluded that LBW, in combination with high current BMI, seems to be of particular importance in the development of high BP.[46]

While the relationship has been detected at different ages, the strength of the inverse relationship increases with age such that among 64–71 years old, systolic BP was decreased by 5.2 mm Hg for each kilogram increase in weight at birth.[14],[19],[47] Law et al concluded that essential HTN is initiated in fetal life.[19],[48],[49] A raised BP is then augmented from early child period to old age, perhaps by a positive feedback mechanism[19],[48],[49] that progressively changes the structure or compliance of blood vessels. The vascular structure and compliance change with hemodynamic load with an increase in peripheral resistance and pulse pressure in early life could alter the structure and reduce compliance, which in turn would increase pulse pressure.[22] A meta-regression analysis presented evidence for the age-dependent association between birth weight and systolic BP.[24],[50] In addition, the inverse association between birth weight and systolic BP is amplified with age, with longitudinal BP measurements during adulthood, and the association was largely accounted for by current weight.[19],[22],[51],[52] The observation on the age amplification of the effect of birth weight indicates that fetal programming and the increasing burden of unhealthy lifestyle behaviors affect the development of adult HTN synergistically.[53] There are indications that ethnicity may modify the relationship between measures of body size and BP.[54] Ethnic differences in these associations might be due to differences in body composition, a parameter frequently compared between ethnic groups.

Numerous mechanisms interplay in the pathophysiology role in the association between body size and elevated BP. First, obesity and central body fat mass damage microvascular function that, in turn, may lead to the development of HTN. Second, obesity leads to enhanced secretion of inflammatory markers such as adipokines and cytokines, in addition to higher C-reactive protein (CRP) levels; a marker of inflammation which interfere with the normal physiological process, leading to HTN.[55],[56],[57],[58]

Earlier reports in adults and adolescents show that BP tended to be less influenced by BMI in Blacks compared to Whites. Others found a small regression coefficient in the non-Caucasian-Caribbean children, although these were not significantly different from the Dutch. Furthermore, Black-Africans in showed a highly similar association with the Dutch children.[59],[60]

Both cross-sectional and longitudinal studies have investigated the association between BMI and waist-hip ratio or waist circumstance with BP, but rarely considered the use of more directly assessed fat mass.[61] However, others found positive associations between BP and fat mass, which was determined by dual-energy X-ray absorptiometry. In addition, studies using bio-impedance to determine fat mass also found correlations with BP.[62],[63]

Blood pressure mechanisms in low-birth-weight individuals

[Table 1] demonstrates possible physiological attributes for the development of high BP in LBW individuals.[64],[65],[66],[67],[68],[69],[70],[71],[72],[73],[74],[75],[76],[77],[78],[79],[80],[81] Possible mechanisms operating in fetal life that might determine BP include the structural development of resistance arteries, setting of hormone levels, and nephron endowment.[82],[83],[84],[85]
Table 1: Possible physiological attributes for the development of high blood pressure in LBW individuals.

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Of these, nephron endowment seems to have received the most attention so far. A physiological basis for elevation in BP associated with LBW is not clear.

During maternal undernutrition, maternal glucocorticoids increase and this excess exposure of the fetus to maternal GC constitutes at least part of the “programming” stimulus.[59],[60],[61] The kidneys have higher levels of Angiotensin type 1 receptor following exposure to a low-protein diet in utero suggesting a role in the programming of HTN.[73],[74],[75] Receptor stimulation, via hormonal binding, mediates an increase in BP by promoting vasoconstriction.[86],[87],[88]

In addition, a decrease in arterial compliance is associated with elevated BP and HTN.[89],[90] A study of 337 men and women born in the Jessop Hospital, Sheffield, between 1939 and 1940 showed that the elasticity of the aorta was directly related to size at birth, birth weight (pounds); abdominal circumference (inches) and occipitofrontal circumference (inches), among 50-year-old men and women.[70] This decrease in arterial compliance, that is inversely related to pulse wave velocity as measured by transit times of blood flow pressure wave in aorto-iliac and femoro-popliteal-tibial arterial segments, in lower birth weight subjects is probably due to a decrease in the amount of elastin present in the vessel’s wall resulting from in utero effects on vascular elastogenesis.[71]

Nephron and blood pressure

HTN might originate through retarded growth in utero followed by accelerated post-natal growth as a result of good living conditions.[72] Retarded fetal growth leads to permanently reduced cell numbers in the kidney and other tissues, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass. The kidney plays a major role in the regulation of systemic BP. It is also known that BP gets disturbed, in both animals and humans, following kidney resection or experimental reduction of kidney mass.[76]

In 1933, Hayman and Johnson reported a close inverse correlation between nephron number and BP.[91] Weder and Schork postulated that BP increases in parallel with growth to match kidney function to the increased demands of greater body mass.[75] They suggested that where kidney growth lags behind somatic growth, sodium retention is favoured and BP rises, thereby predisposing to HTN.[75] Subsequently, it was suggested that a reduced number of nephrons, either genetically determined or acquired in utero, provides an explanation for retardation of kidney growth.[58]

Keller et al studied the kidneys of 10 patients who had primary HTN and died in accidents.[76] They found that the number of nephrons was reduced in white patients with primary HTN. It is not merely a reduced nephron number that is responsible for HTN, but compensatory maladaptive changes that occur internally when nephrogenesis is compromised [Figure 1].
Figure 1: The relationship between intrauterine under nutrition and impairment of kidney function (↓ leads to).

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Brenner et al hypotheses, during late 1980s, that a low nephron number is a risk factor for high BP in later life. The hypothesis stated that a reduction in the total filtration surface area of the kidneys is associated with a compensatory increase in the single nephron glomerular filtration rate.[9],[83],[85],[92],[93] This reduction of nephron number leads to an adaptive structural change that occur within the nephron including glomerular and tubular enlargement and an increase in the number of glomerular capillaries. Subsequently, the afferent arteriole dilates while the efferent arteriole constricts resulting in an increase in the glomerular capillary pressure. This reduction in the afferent arteriolar resistance further fuels an increased transmittance of systemic BP into the glomerulus.[92],[94],[95],[96] Hence, physiological changes occur that contribute to the development of HTN including increased salt reabsorption, higher volume strokes and cardiac output, and resetting of the pressure-natriuresis curve.[97] Pathological changes such as podocyte detachment and tuft adhesion to Bowman’s capsule have been noted in sclerosed kidneys compensating for hyper-filtration (e.g., secondary to vesicoureteral reflux).[83],[93],[98] Over time, this sclerosis of the glomeruli fuels a vicious cycle resulting in a decreased nephron number, the compensatory glomerular hypertrophy, and the progressive HTN and chronic kidney disease.[9],[83],[85],[92],[93] Nephrons that hypertrophied get atrophy sooner, causing further decrease in the number of nephrons.[9],[83],[85],[92],[93] Patients with high BP had almost 50% less number of glomerular number compared to that of the normotensive individuals.[94]

In conclusion, much epidemiological and laboratory evidence suggests that LBW is a risk factor for the development of HTN. However, most studies found significant results when adjustment made for BMI and without considering other factors such as smoking status, alcohol intake, physical activity and socioeconomic status. Oman, like many developing countries, has very high prevalence of NCD and similarly has very high LBW. Hence, determining the mechanisms of HTN that may result from fetal programming is critical in reducing the incidence of future HTN. Most importantly, health care provision to mother and fetus is of great importance to ameliorate the development of LBW. Utmost importance as well, is the provision of life long surveillance of risk factors and markers of development of NCD including HTN in this specific group of population to enable early health care strategy to be instituted to further reduce the burden of disease and provide cost-effective medical strategies.

Conflict of interest: None declared.



 
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Correspondence Address:
Issa Al Salmi
Department of Renal Medicine, The Royal Hospital, Muscat
Oman
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DOI: 10.4103/1319-2442.256836

PMID: 31031365

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