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a Chapter 15 Pulsed Doppler Ultrasonography of the Human Fetal Renal Artery 219
Fetal Renal Artery Doppler Studies
and Intravascular Transfusion
Animal data indicate that renal blood flow is increased
during the first hour after volume expansion
with maternal whole blood [35]. Mari et al. evaluated
the PI of the renal artery waveform from nine anemic
fetuses before and after intravascular transfusion
[36]. The PI of the fetal renal artery decreased within
the first 2 h after intravascular transfusion. The
authors speculated that these observed changes represented
a fall in renal vascular resistance to accommodate
and eliminate the excess infused fluid. Such decreases
in the PI have also been reported immediately
after intravascular transfusion [37].
Fetal Renal Artery Doppler Studies
and Maternal Drug Intake
Indomethacin
Indomethacin has been found useful for the treatment
of preterm labor and in women whose pregnancies
are complicated by polyhydramnios [40]. Treatment
in utero may cause premature ductal closure,
tricuspid insufficiency, and pulmonary hypertension
[41]. Such potentially serious complications have significantly
reduced its routine use in obstetrics.
Indomethacin has been found to cause a significant
increase in fetal renal vascular resistance and a
decrease in renal blood flow [42]. Using PW Doppler
ultrasound Mari et al. studied the fetal renal blood
flow velocity waveforms in 17 fetuses prior to and
24 h after maternal intake of indomethacin [43]. They
found no significant differences in the PI values before
and during indomethacin therapy [43]. These
authors speculated that the decrease in urine production
observed in the fetus during maternal intake of
indomethacin was vasopressin-mediated and not secondary
to increases in renal vascular resistance. This
important observation must be confirmed by additional
studies.
Van Bel et al. studied the effect of a single dose of
intravenous indomethacin on renal blood flow velocity
waveforms. Using color PW Doppler imaging on
15 premature infants, they found that a single dose of
intravenous indomethacin led to a sharp decrease in
peak systolic and temporal mean flow velocities [44].
These effects were maximal 10 min after the indomethacin
dosing.
Aspirin
Aspirin, a potent antiinflammatory drug, has been
shown to inhibit the biosynthesis and release of prostaglandins,
even in low dosage. This observation led
many researchers to speculate that the ingestion of
daily low-dose aspirin may result in a decrease in the
incidence of preeclampsia and fetal growth restriction,
and that it may improve pregnancy outcome in
women with positive lupus anticoagulant and anticardiolipin
antibodies [45, 46].
Veille et al. studied the effect of prolonged maternal
ingestion of low-dose aspirin on the fetal renal
circulation [47]. They could demonstrate no significant
hemodynamic changes in the fetal renal Doppler
waveforms in fetuses chronically exposed to low-dose
aspirin compared to a group of fetuses not exposed
to such medication. Thus the prolonged use of lowdose
aspirin in the human fetus does not seem to significantly
affect fetal renal circulation.
Ritodrine
The effects of intravenous ritodrine infusion on the
fetal renal artery waveforms of eight singletons were
assessed by Rasanen [48]. The fetal renal artery waveforms
were examined prior to ritodrine and after
2.5 h of infusion. Ritodrine decreased the Doppler
waveform indices of the renal arteries, suggesting a
decrease in vascular resistance of these vessels [48].
Angiotensin-Converting Enzyme Inhibitors
The angiotensin-converting enzyme (ACE) inhibitors
have been used to treat hypertensive disorders during
pregnancy. Such treatment can severely and sometimes
definitively impair renal function in the fetus,
leading to postnatal anuria [49]. Evidence from the
published literature suggests that the primary mechanism
by which ACE inhibitors affect development of
the fetal kidney is through decreasing the renal blood
flow [50] and their interference between the renin-angiotensin
system and the prostaglandins.
Table 15.3 shows the effects of maternal medication
on fetal renal blood flow.
Table 15.3. Effects of maternal medication on fetal renal
blood flow
Maternal drugs Effect on fetal Reference
renal artery
ACE inhibitors Decrease in PI Martin RA [50]
Aspirin No change Veille JC [47]
Betamethasone No change in PI Edwards A [51]
Cyclooxygenase-2 No change Holmes RP [52]
inhibitor
Ibuprofen No change Romagnoli C
[53]
Indomethacin PI is increased Kang NS [54]
Intravaginal No change Wang Z [55]
Misoprostol
Ritrodrine No change Rasanen J [48]
Terbutaline No change Kramer WB [56]