o_1977r8vv9vk1ts2ms0kd8pksa.pdf

218 J. C. Veille
response to hypoxia [31]. Hypoxia caused the fetal
carotids to contract, whereas the same degree of hypoxia
caused the fetal renal arteries to relax. In vivo
studies suggest that the same vessel responds differently
within its length. For example, the proximal
carotid of the fetal guinea pig constricts, whereas the
distal carotid relaxes under the same hypoxic conditions
[31].
Such regional differences are supported by observations
in the fetal circulation of normal human fetuses.
Normal women during the third trimester of
pregnancy were asked to inhale a gas mixture containing
3% CO 2 [32]. The responses of the umbilical,
middle cerebral, and renal arteries were analyzed before
and during the 15-min CO 2 challenge. A significant
decrease in the S/D velocity ratio occurred in
the fetal middle cerebral artery but not in the fetal renal
artery or the umbilical artery [32]. The authors
concluded that human fetal vessels can selectively
vary their resistance with the same stimulus, supporting
the vascular differences previously reported for
guinea pigs.
One study looked at two groups of pregnancies resulting
in intrauterine chronic hypoxia in the third
trimester. Group 1 comprised 120 pregnant women
with pregnancy-associated hypertension and/or proteinuria.
Group 2 consisted of 87 pregnancies with
IUGR. Both study groups included pregnant women
in the third trimester. Hyperechogenic renal medullae
were detected in 15 out of 120 cases with pregnancyassociated
hypertension and/or proteinuria, and in 22
fetuses of the 87 pregnancies involving IUGR [33].
Fetal renal hyperechogenicity appears to be an indicator
of fetal arterial circulatory depression, correlated
with pathological changes in the RI for the fetal
renal arteries. The fetal renal arterial blood flow RI
was significantly lower in hyperechogenic cases. The
authors concluded that these findings may represent
an indication of subsequent intrauterine and neonatal
complications. In such fetuses cesarean section was
increased because of intrauterine hypoxia. In those
with fetal renal hyperechogenicity there was an increase
in fetal distress (43%), admission to a neonatal
intensive care unit (51%), and an increase in perinatal
mortality (5.4%, as compared with 0.8%±1.0% in
the normal population). They concluded that a detailed
ultrasound and Doppler examination of renal
parenchyma and arteries may be a useful method
prenatally to diagnosis fetal reduced renal perfusion
[33].
Fetal Renal Artery Doppler Studies
and Postterm Pregnancy
Arduini and Rizzo reported on the PI of 97 patients
with gestational ages of more than 42 weeks [16].
They found no significant differences in the fetal renal
artery PIs for postdate pregnancies when compared
to a group of normal fetuses studied between
weeks 40 and 42 of gestation, even when these postterm
pregnancies had decreased amniotic fluid volume.
In a study done on 50 patients with prolonged
pregnancies Veille et al. found that the S/D ratio was
significantly higher in prolonged pregnancies complicated
by oligohydramnios [34]. These authors also
found a significant negative correlation between the
amniotic fluid index and the fetal renal S/D ratio
[34]. Animal and human data indicate and support
the notion that moderate to severe hypoxia significantly
affects renal blood flow and renal vascular impedance
[35, 36]. Since the introduction of the color
Doppler technique, small vessels such as the fetal renal
arteries can be effectively studied. With technical
improvement and standardization of the pulsed Doppler
acquisition, studies using such noninvasive
methods contribute to our understanding of fetal regional
circulation during normal and abnormal development.
The amniotic fluid decreases with advancing gestation
in the face of an increase in cardiac output and
an increase in renal perfusion. The etiology of oligohydramnios
in normally grown fetuses who are born
postterm has been studied using Doppler velocimetry.
Recently, Oz obtained the RI of the renal and umbilical
artery Doppler velocimetry in 147 singleton postterm
fetuses (287 days or more of gestation) [37]. The renal
artery RI was significantly higher in cases with oligohydramnios
[RI: mean (Ô standard error) = 0.8843
Ô 0.11 versus 0.8601Ô0.05, P£0.05]). A renal artery
Doppler end-diastolic velocity below the mean for gestation
significantly increases the risk of oligohydramnios.
These authors concluded that an elevated renal artery
Doppler RI was more predictive of oligohydramnios
than the umbilical RI. They went on to speculate
that a reduced renal artery end-diastolic velocity suggests
an increase in arterial impedance and that this
may be an important factor in the development of oligohydramnios
in prolonged pregnancies [37].
We previously noted that postterm fetuses with oligohydramnios
and evidence of fetal acidosis had a
significant increase in the RI of the fetal renal artery
when compared to a group of fetuses that were also
postterm and had oligohydramnios [38]. Scott et al.
[39] had similar findings, that the PI of the renal artery
was higher in normally grown fetuses with oligohydramnios
when compared to those with normal
amniotic fluid. These investigators also found that
those fetuses who were growth restricted and had oligohydramnios
had significant PI values of the fetal
renal arteries.