Pediatr Nephrol (2011) 26:119–126
DOI 10.1007/s00467-010-1646-3
ORIGINAL ARTICLE
Ambulatory blood pressure monitoring and renal functions
in term small-for-gestational age children
Ilmay Bilge & Sukran Poyrazoglu & Firdevs Bas &
Sevinc Emre & Aydan Sirin & Selman Gokalp &
Sema Eryilmaz & Nezih Hekim & Feyza Darendeliler
Received: 20 January 2010 / Revised: 17 June 2010 / Accepted: 26 July 2010 / Published online: 2 October 2010
# IPNA 2010
Abstract The aim of this study was to investigate the
relationship between birth weight and blood pressure (BP) by
means of ambulatory BP monitoring (ABPM) and renal
functions in non-obese children who were born small-for-
gestational age (SGA) at term. The study group consisted of
39 (19 female, 20 male; mean age 8.8±2.6 years) children
born SGA. Their data were compared to those of 27 (13 female,
14 male; mean age 8.2±2.9 years) children born appropriate-
for-gestational age (AGA). No difference between SGA and
AGA children was observed based on office BP measurements
and daytime, nighttime and 24-h ABPM. Seventeen SGA
(48.6%) and nine AGA (37.5%) children had a 24-h systolic
BP (SBP) load over 25%, and seven of these (5 SGA, 2 AGA)
were hypertensive according to mean SBP values. The
prevalence of the non-dipping phenomenon in SGA and
I. Bilge : S. Emre : A. Sirin
Department of Pediatrics, Pediatric Nephrology Unit,
Istanbul Faculty of Medicine, Istanbul University,
Çapa-Istanbul 34390, Turkey
S. Poyrazoglu : F. Bas : S. Eryilmaz : F. Darendeliler
Department of Pediatrics, Pediatric Endocrinology Unit,
Istanbul Faculty of Medicine, Istanbul University,
Çapa-Istanbul 34390, Turkey
S. Gokalp
Department of Pediatrics, Istanbul Faculty of Medicine,
Istanbul University,
Çapa-Istanbul 34390, Turkey
N. Hekim
Dr. Pakize I. Tarzi Laboratory,
Istanbul, Turkey
F. Darendeliler (*)
Çocuk Kliniği, İstanbul Tıp Fakültesi,
Çapa-Istanbul 34390, Turkey
e-mail: feyzad@istanbul.edu.tr
AGA children was similar. Renal functions were normal and
similar in both groups. Three children (2 SGA, 1 AGA) with
normal glomerular filtration rate had higher microalbumin
excretion and one SGA child had systolic hypertension
according to the office BP. Our findings demonstrate that the
influence of intrauterine growth restriction on BP is not
manifested during the childhood period, and they do not
support the existence of a negative relationship between birth
weight and BP in children.
Keywords Small-for-gestational age (SGA) .
Ambulatory blood pressure monitoring . Hypertension .
Children . Microalbumin . Beta-2 microglobulin .
Beta-N-acetyl-D-glucosaminidase
Introduction
The fetal programming hypothesis suggests that an adverse
intrauterine milieu causes structural, hormonal and metabolic
adaptations in the fetus that persist in later life. Term babies
who are small-for-gestational age (SGA) have been shown to
develop insulin resistance and other comorbidities, including
type 2 diabetes mellitus, hyperlipidemia, hypertension and
coronary heart disease in adult life [1]. In addition to the
adverse intrauterine environment, postnatal catch-up-growth
(CUG) has also been implied as playing a role in the
developing morbidities [2]. Insulin resistance, the hallmark
of these abnormalities, is an early pathology that starts in early
childhood in children who were born SGA. Rapid growth,
especially in the first 2 years of life, contributes to insulin
resistance, particularly if accompanied by an increased body
mass index (BMI) [3].
Several physiological, biochemical, genetic and environ-
mental factors are known regulators of blood pressure (BP)
120
in humans. Intrauterine growth restriction may also be
responsible for the prenatal programming of BP. A number
of studies have shown an association between low birth
weight and higher BP in later life [4–6], but others did not
provide support for fetal origin hypothesis as applied to BP
regulation, reporting that the association between birth size
and later blood pressure was not significant [7–9].
Ambulatory blood pressure monitoring (ABPM) has been
increasingly used to investigate hypertension in different
pediatric populations. However, there are only a few reports
on ABPM, microalbuminuria and renal functions in SGA
children [10–13], and the utility of BP in SGA children has
not been well established. Therefore, the aim of this study was
to investigate the relationship between birth weight and BP
parameters by applying ABPM and evaluating microalbumi-
nuria and renal functions in a group of non-obese children
born SGA and comparing their data to those of control
children born appropriate-for-gestational age (AGA).
Patients and methods
The study group consisted of 39 (19 female, 20 male) children
born SGA with a birth weight and/or length < −2 standard
deviations (SD) for gestational age. The children were born at
term (>36 6/7 weeks of gestational age, when nephrogenesis is
regarded as to be completed [14]). All of the SGA children
followed were from our Pediatric Unit. Those who are born at
our hospital, with a gestational age >36 6/7 weeks and with a
precise birth weight and those who made a CUG and were
prepubertal and non-obese were included in the study. Those
who had a chronic disease, congenital malformation or genetic
disease and a renal disease or previously documented urinary
tract infection were excluded from the study. The lower age
for inclusion was 3 years to allow for CUG and the upper
limit was <13 years in girls and <14 years in boys (upper
limits of normal pubertal age) and with no signs of puberty.
We included SGA children with no major abnormalities in the
intrauterine period. Age-matched non-obese healthy children
from the Well Child Unit who were being followed mainly for
growth monitoring comprised the control group. The children
of both the SGA and AGA groups were Caucasian and came
from families of similar socioeconomic status.
The mean age of the SGA children at the time of
investigation was 8.8±2.6 years (range of 5.6–12.4 years).
Their data were compared to those of 27 healthy AGA-born,
age-matched, non-obese children of normal height (13 female,
14 male). The mean age of the AGA children at the time of
investigation was 8.2±2.9 years (range 5.5–12.2 years). All
children had BMI within normal ranges. Medical histories
regarding gestational age, weight and length at birth were taken
from the hospital files. Gestational age was determined
primarily by the mother’s last menstrual period.
Pediatr Nephrol (2011) 26:119–126
Family history with regard to hypertension and kidney
disease was recorded. In no cases was there a history or
family history that suggested renal disease.
Following a thorough physical examination, anthropometric
measurements, including height and weight, were taken by
standard methods using the Harpenden stadiometer. The BMI
was calculated as weight (kg)/height (m)2. Values of height and
weight [15], BMI [16] and birth weight and length [17] were
expressed as the standard deviation score (SDS). Δ height
SDS was defined as the difference (Δ) between birth length
SDS and current height SDS, and Δ weight SDS as the
difference (Δ) between birth weight and current weight SDS.
Target height (TH) was calculated from parental height
[father’s height (cm) + mother’s height (cm)]/2 − 6.5 cm
(girls), + 6.5 cm (boys). Birth data and the measurements of
the children at investigation are shown in Table 1.
BP measurements
Office BPs were measured using the oscillometric portable
pediatric device Dinamap (Critikon Corp, Tampa, FL) with an
appropriate cuff size for all children. The BP was measured
three times under resting conditions, and the mean value of the
three measurements was used in the analysis. Hypertension was
defined as either a systolic (SBP) or diastolic BP (DBP) higher
than the 95th percentile for sex, age and height. Normal values
were taken from published data [18].
ABPM was performed using an oscillometric device
(Mobil-O-Graph; SpaceLabs, Diessenhofen, Switzerland).
Measurements were taken automatically in the non-
dominant arm at 15-min intervals during the daytime and at
30-min intervals during the night. Daytime was defined as
0800–2000 hours and nighttime as 0000–0600 hours. Chil-
dren were advised to maintain their usual activities but to
avoid vigorous exercises when wearing the monitor. The
monitors recorded the time the children went to bed and the
time they awoke as well as the exercise periods. A minimum
of 22 h of recording time and at least 40 recordings were
required for an adequate ABPM profile. The ABPM records
were downloaded to a PC-compatible computer and analyzed
by the SpaceLabs software computer program for mean heart
rate (HR), SBP and DBP during sleep or when awake over the
24-h period, percentage of nocturnal decline of SBP and DBP
and BP loads. The percentage nocturnal decline (% N fall) of
SBP and DBP was calculated as: [(mean daytime BP − mean
nighttime BP)/mean daytime BP] × 100. The nocturnal
threshold was 10% less than the limits when awake. BP loads
were accepted as the percentage of systolic BP and diastolic
BP readings greater than the 95th centile for a given time
period. We classified BP as normal if the mean ambulatory BP
was <95th percentile and the BP load was <25%.
Because BP changes with age, gender and height,
standardized scores were calculated to facilitate the com-
Pediatr Nephrol (2011) 26:119–126 121

Table 1 Anthropometric parameters of the SGA and AGA children at birth and at the time of the study

Anthropometric parameters SGA (n=39) AGA (n=27) p

Gender (girl/boy) 19/20 13/14 1.0

Family history for HT 9 6
At birth
Gestational age (weeks) 39.4±1.1 39.3±1.4 0.74
Birth length (cm) 45.0±3.3 49±3.0 0.001
Birth length SDS −2.4±1.5 −0.5±1.1 0.001
Birth weight (g) 2170.8±362.7 3121.0±389.8 0.001
Birth weight SDS −3.2±0.8 −0.7±0.9 0.001
At investigation
Age (years) 8.8±2.6 8.2±2.9 0.35
Height SDS −1.5±0.5 −0.9±0.7 0.001
Weight SDS −1.4±0.8 -1.0±0.9 0.19
BMI 15.6±3.0 16.2±2.5 0.37
BMI SDS −0.8±0.7 −0.5±0.8 0.24
Target height SDS −1.1±0.4 −0.8±0.7 0.04

Values are given as the mean ± standard deviation (SD)

SGA, Small-for-gestational age; AGA, appropriate-for-gestational age; HT, hypertension; SDS, standard deviation score; BMI, body mass index

parison of the data obtained on our study population with
those of the general pediatric population using a published
formula for office BP and ABPM [18, 19].
Renal functions were evaluated in all children. Urinary
proteins used as markers of glomerular damage due to
hyperfiltration and of tubular damage were analyzed. After
an overnight fast, serum samples were drawn for serum
urea and creatinine (Cr). Early morning urine was collected
from the children of both the SGA and AGA groups, and
the samples were kept at −20°C until analyzed for micro-
albumin, urinary beta-2 microglobulin (U-B2M), urinary
beta-N-acetyl-D-glucosaminidase (UNAG) and urinary Cr.
All patients had a normal renal function defined as a
glomerular filtration rate (GFR) of >90 ml/min/1.73 m2 (as
determined by the Schwartz formula) [20].
Methods
The serum Cr level was determined by the Jaffe method
(COBAS INTEGRA 800; Roche, Branchburg, NJ). Urine
creatinine and UNAG measurements were performed by the
colorimetric method (COBAS INTEGRA 800; Roche). Urine
albumin and U-B2M were measured by nephelometry using a
Behring BN ProSpec analyzer (Dade Behring, Milton Keynes,
UK). Microalbumin, UNAG and U-B2M levels were
expressed as a ratio to the urine Cr concentration.
Statistical analysis
All data were stored and analyzed using the SPSS 12
statistical package (SPSS, Chicago, USA). Values are
expressed as the arithmetic mean ± SD. Comparisons were
performed between the groups using parametric tests as
appropriate. The chi-square test was applied for the compar-
ison of prevalence between groups. Pearson's correlation test
was used to analyze BPs in relation to anthropometric
variables. In the multiple regression analysis, office and
ambulatory BP SDS values and renal function tests were
taken as dependent variables in separate models, and birth
size, gender, age, Δ height SDS, Δ weight SDS and recent
BMI SDS were taken as independent variables and tested in
each of these models. In the logistic regression analysis, we
also used birth weight to predict the prevalence of
hypertension, BP loads and the non-dipper in unadjusted
models; in the multivariable logistic analysis, we included
age, gender, Δ weight SDS, Δ height SDS and BMI SDS as
independent variables. Significance was set for p<0.05.
Ethics statement
This study was approved by the local ethical committee.
Informed consent was obtained from the parent(s) of both
the cases and the controls.
Results
Anthropometry
The anthropometric parameters of the SGA and AGA
children at birth and at the time of the study are given in
Table 1. The mean gestational age, mean age at the time of
122 Pediatr Nephrol (2011) 26:119–126

the study, sex and family history for hypertension of the
children of both groups were not different. By definition,
birth weight, length and SDS’s were significantly lower in
SGA children than in AGA children (p<0.001). At the time
of the investigation, weight SDS and BMI SDS fell within
normal limits and were similar in both groups. Although
SGA children were shorter than AGA children (p=0.01),
their height SDS corrected for their parents was within
normal limits (0.4±0.2). Δ height SDS and Δ weight SDS
were 1.1±0.9 and 1.8±0.9 in the SGA group and −0.1±0.8
and −0.2±0.7 in the AGA group, respectively.
BP parameters of SGA and AGA children
There was no gender difference in the mean values of BP,
so the data for boys and girls are presented together.
No difference between SGA and AGA children was
observed in terms of hypertension based on the office BP
measurements (Table 2).
A satisfactory ABPM profile was obtained in 59 (89.4%)
of all children. In five children there were fewer than 40
satisfactory recordings, while in two children the recording
time was shorter than 22 h due to device discomfort. The
mean of ABPM records was 52 (range 22–76).
The mean heart rates did not differ significantly between
the children in the SGA and AGA groups at any time point. In
addition, there were no differences in office, the 24-h, daytime
and nighttime SBP and DBP between the groups (Table 2).
The frequencies of systolic and/or diastolic hypertension in
the children of the SGA and AGA groups according to daytime,
nighttime and 24 h ABPM were similar and did not show
significant differences based on these parameters (Table 3).
The mean day to night fall (dipping) in SBP and DBP
was similar in both groups (14.04±5.8% and 12.8±7.8 for
SBP and 16.7±7.3% and 14.2±7.9% for DBP in SGA and
AGA children, respectively). The prevalence of the non-
dipping phenomenon was not significantly different in SGA
and AGA children (Table 3).
Correlations
No significant correlations were observed between the birth
weight, birth length, SDS’s and office and ABPM param-
eters in the children of the SGA and AGA groups.

Table 2 Heart rates and blood pressure of children in the SGA and AGA groups

Heart rates and blood pressure parameters SGA AGA p

Office BP
Systolic BP (mmHg) 102.2±11.2 103.1±9.6 0.73
SDS 0.5±0.8 0.5±0.7 0.28
Diastolic BP (mmHg) 66.4±11.8 62.8±8.3 0.17
SDS 0.7±0.6 0.5±0.7 0.24
Mean heart rates
24 h (beats/min) 89.2±12.04 90.3±12.8 0.74
Daytime (beats/min) 94.5±12.2 95.9±11.9 0.66
Nighttime (beats/min) 77.6±15.1 78.8±16.1 0.77
Systolic ABPM
24 h (mmHg) 103.2±8.7 103.5±9.3 0.89
SDS −0.2±0.7 −0.1±0.6 0.60
Daytime (mmHg) 107.6±8.8 108.5±9.6 0.70
SDS −0.5±0.8 −0.4±0.9 0.71
Nighttime (mmHg) 92.6±7.9 94.9±8.1 0.34
SDS −0.2±0.8 −0.1±0.8 0.70
Diastolic ABPM
24 h (mmHg) 62.2±6.7 62.1±5.7 0.95
SDS −0.7±0.8 −0.7±0.7 0.94
Daytime (mmHg) 64.4±7.2 65.9±5.8 0.79
SDS −0.9±0.8 −0.9±0.7 0.91
Nighttime (mmHg) 56.6±4.9 58.2±5.9 0.27
SDS −0.5±0.6 −0.6±0.7 0.58

Values are given as the mean ± SD

BP, Blood pressure; ABPM, ambulatory BP monitoring
Pediatr Nephrol (2011) 26:119–126 123

Table 3 The frequencies of hypertension and blood pressure loads in Renal functions and biochemical evaluation
the SGA and AGA groups [n (%)]

Parameters SGA (n=35) AGA (n=24) p As shown in Table 4, serum Cr and urea concentrations
were normal in all children of both the SGA and AGA
Office BP children, and they were not different between the groups.
Systolic hypertension 3 1 0.63 According to the Schwartz formula, all children had a
Diastolic hypertension 3 0 0.26 normal GFR. The prevalence of microalbuminuria was
ABPM daytime similar in both the SGA [5.1% (2/39)] and AGA [3.7% (1/
Systolic hypertension 9 6 1.0 27)] groups (p=0.9). However, three children (2 SGA, 1
Diastolic hypertension 1 0 1.0 AGA) with normal GFR had higher microalbumin excre-
Systolic BP load 21 12 0.61 tion (30–300 mg/g Cr) and only one of the SGA children
Diastolic BP load 4 1 0.64 with microalbuminuria had systolic hypertension based on
ABPM nighttime the office BP measurements.
Systolic hypertension 1 1 1.0 The GFR was not correlated with birth weight, birth
Diastolic hypertension 1 0 1.0 weight SDS, Δ weight SDS, BMI, BMI SDS and blood
Systolic BP load 6 9 0.13 pressure parameters. Microalbuminuria, NAG and B2M
Diastolic BP load 1 2 0.56 excretion were also not correlated to birth weight, birth
ABPM 24 h weight SDS, Δ weight SDS, BMI and BMI SDS.
Systolic hypertension 5 2 0.68
Diastolic hypertension 1 0 1.0
Systolic BP load 17 9 0.43 Discussion
Diastolic BP load 3 1 0.63
Nocturnal non-dipping status Results of epidemiological studies have linked low birth
Non-dipper 8 8 0.39 weight to a raised BP in adult life, but very little data are
Systolic 7 7 0.53 available on the effect of birth weight on cardiovascular
Diastolic 6 6 0.52 dynamics and BP during childhood. Therefore, in this
prospective analysis, we have evaluated the possible
relationship between birth weight and BP parameters by
applying ABPM in 35 non-obese children born SGA and
Similarly, current height SDS, weight SDS and BMI SDS compared their data to those of 24 children born AGA. The
did not show any correlation with any of the office and results of our study do not support the existence of a
ABPM parameters in both groups. negative relationship between birth weight and BP in non-
In a linear regression analysis, office and ABPM were obese prepubertal children born SGA at term.
not associated with birth weight, birth weight SDS, Δ It has been suggested that low birth weight may have a
weight SDS and BMI SDS, all adjusted for gender. The long-term impact on the individual’s health, with an
logistic regression analysis did not reveal an independent increased risk of hypertension, cardiovascular events and
relation between office and ABPM and any parameter. altered renal function in adult life [21]. Although the

Table 4 Renal functions of the children born SGA and AGA at term at the time of the investigation

Renal markers SGA (n=39) AGA (n=27) p

Urea (mg/dl) 26.0±7.5 24.8±5.2 0.47

Creatinine (mg/dl) 0.3±0.1 0.4±0.1 0.94
Urine
B2MG/creatinine (μg/g) 51.1±30.9 44.3±26 0.41
NAG/creatinine (IU/g) 5.4±2.0 5.0±2.1 0.55
Microalbuminuria/creatinine (mg/g) 20.7±13.8 20.6±11.1 0.91
GFR 129.7±27 133.1±24.8 0.70

Values are given as the mean ± SD

B2MG, Beta-2 microglobulin; NAG, β-N-acetyl-D-glucosaminidase; GFR, glomerular filtration rate
124
pathogenesis is still unclear, it has been proposed that fetal
growth retardation may be associated with impaired
nephronogenesis, resulting in fewer nephrons and an
increased chance of renal disease later in life. Glomerular
hyperfiltration resulting from a reduced number of neph-
rons could lead to systemic hypertension, glomerular
sclerosis and progressive deterioration of renal function
[22]. Nephrogenesis is a complex process that requires
many factors. Epigenetic changes lead to stable and
potentially heritable changes in gene expression. The
environmental impact on a genetic program may act on
the specific genetic programming of low nephron number.
This phenomenon may suggest an epigenetic effect of
perinatal factors on the development of diseases later in life.
Epigenetic changes, especially methylation, have been
strongly implicated in fetal renal development and diseases
which appear at a later date [22]. Potential important factors
influencing nephrogenesis may include activation of the
renin–angiotensin–aldosterone system, an increase in the
gene expression of various tubular sodium channels,
significant reduction of enzyme 11 beta- hydroxysteroid
dehydrogenase type 2 gene and fetal glucocorticoid excess,
hyperactivation of the sympathetic nervous system, inhibi-
tion of nitric oxide and insulin-like growth factor I and
increased serum uric acid level [23].
Many studies in adults have shown that individuals who
were small at birth tend to have higher BP in later life and
there is an inverse relationship between size at birth and
SBP later in life [24]. There is conflicting evidence on the
prevalence of hypertension in children born SGA. In a
cohort of 891 children, there was no evidence to suggest
that children with a low birth weight who became
overweight and obese had extra high BP [7]. In a large
bi-racial U.S. cohort, children who were SGA at term did
not have a greater risk of developing high BP at 7 years of
age [8]. Rakow et al. [9] reported that BP did not differ
between children born SGA at term and those born AGA at
term at a mean age of 9.8 years. Keijzer et al. [10] showed
that very premature birth increases SBP in young adults but
that intrauterine growth retardation does not seem to
attenuate this effect. In our study, mean BP level in children
born SGA and AGA at term was similar. Although the
prevalence of hypertension and elevated SBP loads were
high, there was no significant difference between SGA and
AGA children. Larger SGA and AGA groups may be
needed in future studies. In contrast, in study carried out in
Israel, 58 children aged 4–6 years with intrauterine growth
retardation had a significantly increased BP compared with
normal birth children (controls) [4]. Similarly, in a
longitudinal study with children aged 5 through 21 years,
birth weight was consistently inversely associated with SBP
from childhood to young adulthood and to DBP in young
adulthood [5]. Bayrakcı et al. [6] described abnormal
Pediatr Nephrol (2011) 26:119–126
circadian BP regulation in SGA preterm children aged
between 5 and 17 years. Selective increase in the nocturnal
SBP is prominent in children with intrauterine growth
retardation.
It has been suggested that postnatal adaptations in
growth, rather than intrauterine growth restriction itself, is
associated with an increased BP in adolescence [2, 25]. In
their longitudinal study from birth to 22 years of age, Law
et al. [26] showed that the lower birth weight and greater
CUG rate were associated with systolic hypertension in
young adult life. In a large bi-racial U.S. cohort, children
who crossed weight percentiles in the upward direction
were found to be at an increased risk for high BP, but the
magnitude of the effect of weight gain on BP did not
depend on size at birth [8]. Williams et al. [7] reported that
there was no evidence to suggest that children with a low
birth weight who became overweight or obese had extra
high BP. In a large cohort of children aged 5–8 years,
Bergel et al. [27] found no overall association between birth
weight and BP in childhood. Nevertheless, among over-
weight children, BP was higher in those with a low birth
weight than in others. Our study included only non-obese
children. In our children, the lack of association between
BP and birth weight and CUG may be due to the normal
ranges of BMI in our children.
Microalbuminuria reflects the increase in glomerular
vascular permeability which can precede the eventual
decrease in GFR [28]. NAG is located in lysosomes of
the proximal tubular cells, and damage to these cells leads
to an increase in urinary NAG excretion. B2M, a low-
molecular-weight protein, is freely filtered from the
glomerular basement membrane and is almost completely
reabsorbed from the proximal tubular epithelial cell by
endocytosis and catabolized by lysosomal enzymes. The
level of urinary B2M increases with proximal tubular
damage and dysfunction. UB2M and UNAG excretion
have been used as markers of tubulointerstitial damage and
dysfunction [29]. Subtle tubular disturbances have been
reported in children and adults born SGA [30, 31]. Monge
et al. [32] observed elevated NAG excretion in children
aged 4–12 years who had been born with a low birth
weight. It has been reported that the GFR is significantly
diminished and there is increased microalbuminuria in
young adults who were born preterm with intrauterine
growth retardation [11]. Iacobelli et al. [33] suggested that
in premature very low birth weight infants, acute con-
ditions, such as early CUG, may affect renal outcome in an
unfavorable way. Rakow et al. [9] showed that there was no
significant difference in renal function between children at
9 years of age who had been born SGA at term and those
born AGA at term and that thee was no sign of glomerular
and tubular damage in the SGA children. In our study, renal
function and urinary protein excretion were similar in the
Pediatr Nephrol (2011) 26:119–126
children born SGA and AGA at term. The GFR and protein
excretion was not associated with birth weight, CUG and
BP.
A major limitation to our study may be relatively low
number of children born SGA at term. However, our aim
was to select a homogenous group of SGA children who
were born at term, were non-obese and prepubertal at the
time of the investigation. All children had gestational ages
greater than 36 6/7 weeks. Thus, nephron formation and the
number of nephrons were considered to be completed
before birth.
In summary, our findings do not demonstrate the
presence of an influence of intrauterine growth retardation
on BP in young children born SGA at term. Although the
ability to predict a child’s risk for hypertension would be of
considerable benefit in identifying those who may need
more intensive monitoring and risk-factor intervention,
limited information is available regarding the main risk
factors in SGA children. School-age children born SGA
who have normal kidney function, even if they make a
CUG, but do not become obese have normal BP values
during childhood. With respect to previous studies showing
that intrauterine growth retardation and excessive weight
gain may be associated with systolic hypertension and
subtle deterioration of kidney functions, we suggest that
such relationships have to be confirmed in other prospec-
tive studies on larger populations before these results can be
extrapolated to the general population. We also suggest that
long-term follow-up of all children born SGA is warranted.
Acknowledgments We would like to express our gratitude to
NovoNordisk, Turkey for providing financial support for purchasing
the kits.
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