Pediatr Nephrol (1999) 13:938–944
P R A C T I C A L P E D I AT R I C N E P H R O L O G Y
Pierre D.E. Mouriquand · Eric Troisfontaines
Duncan T. Wilcox
Antenatal and perinatal uro-nephrology:
current questions and dilemmas
Received: 13 February 1998 / Revised: 30 July 1998 / Accepted: 8 October 1998
Abstract The development of antenatal ultrasonography
and the detection of fetal uropathies has created a new
field for paediatric urologists. The embryology and phys-
iology of the fetal renal tract is still poorly understood. It
is, however, recognised that delays in the maturation of
the renal system can lead to transient dilatation of the
urinary tract. Structural and functional anomalies can
also result in dilatation, but these are permanent. The
ability to distinguish between the transient and perma-
nent impairments to urine flow represents a diagnostic
challenge. This review article discusses the pathophysi-
ology of urine flow impairment, antenatal detection and
the postnatal management of the common congenital
uropathies.
Key words Antenatal · Urology · Uropathy ·
Hydronephrosis · Pelvo-ureteric junction ·
Posterior urethral valves · Urine flow impairment
Introduction
For nearly 20 years, antenatal ultrasound scanning, bio-
chemical analyses of fetal urine and experimental studies
have revealed data on the construction and function of
the fetal urinary tract. The antenatal detection of dilated
urinary tracts has opened up the field of antenatal uro-
nephrology and led to the early diagnosis of congenital
urine flow impairments (UFI). The interpretation of the
antenatal findings and their postnatal management, how-
ever, remain difficult, as our knowledge of the embryolo-
gy and physiology of the fetal urinary tract is still rudi-
mentary. The aim of this article is to review our current
knowledge of the pathophysiology, antenatal investiga-
tions and immediate postnatal management of patients
with antenatally diagnosed uropathies.
P.D.E. Mouriquand (✉) · E. Troisfontaines · D.T. Wilcox
Department of Paediatric Urology, Great Ormond Street
Children’s Hospital NHS Trust, Great Ormond Street,
London WC1N 3JH, UK
Tel.: +44-171-405-9200
© IPNA 1999
Pathophysiology of UFI
The kidney’s response to a UFI can be described in terms
of both its structure and function. The structural response
is related to severity, anatomical site and duration of ob-
struction. When UFI occurs early in pregnancy and is
complete, the renal parenchyma becomes dysplastic and
ultimately will undergo apoptosis and atrophy [1–3].
However, when UFI becomes significant at a later date
in gestation or is partial, it causes a dilatation of the ex-
cretory system without affecting the renal parenchyma
[4, 5]. The function of the kidney is also affected: unilat-
eral UFI causes a reduction in ipsilateral glomerular fil-
tration rate (GFR) and an increase in contralateral GFR,
which may become permanent after 6 weeks of complete
obstruction [6]. In addition to a decrease in GFR, tubular
function is affected, with an increased production of hy-
ponatraemic urine and a reduced ability to concentrate
urine in the ascending loop of Henle [7, 8].
Antenatal investigations
Ultrasonography and the biochemistry of fetal urine are
used clinically to follow the development of the fetal uri-
nary tract and to assess congenital UFI.
Ultrasound studies
Ultrasonography examines: (1) the dilatation of the uri-
nary system; (2) the echostructure of the renal parenchy-
ma; (3) the volume of amniotic fluid; and (4) the visuali-
sation of the fetal bladder.
Interpretation of a dilated urinary tract. This can be due
transient UFI. The developing ureter is initially solid and
becomes patent during gestation and the maturation of
the ureter continues postnatally. Therefore a delay in the
maturation of the ureter can result in a transient UFI,

which can improve and/or resolve during later develop-
ment. Dilatation can be related to a permanent UFI. In
that case, the cause of the UFI can be demonstrated after
birth. This is the most-common situation. Finally, dilata-
tion can be secondary to a systemic disorder of the con-
nective tissue of the excretory system (i.e. collagen dis-
orders, prune-belly syndrome) leading to an impaired
transit of urine.
Echostructure of the renal parenchyma. Structural anom-
alies of the fetal kidney can be associated on utrasonogra-
phy with a bright parenchyma, cystic parenchyma, small
kidneys and poor cortico-medullary differentiation.
The volume of amniotic fluid. The assessment of amniot-
ic fluid volume, although subjective, is important, as fe-
tuses with bilateral significant UFIs and/or bilateral ab-
normal kidneys may present with oligohydramnios.
The visualisation of the bladder. Persistent large blad-
ders can indicate a urethral UFI (valve or atresia), a neu-
ropathic bladder or some complex cloacal malforma-
tions. Increased renal echogenicity and oligohydramnios
in the setting of bladder distension and bilateral hydrone-
phrosis are highly predictive of an obstructive etiology
[9]. If the bladder is not visualised this could be a normal
empty fetal bladder, and repeated ultrasound should
demonstrate this, or it can reflect severe pathology, such
as bladder exstrophy, cloacal exstrophy, epispadias, bi-
lateral ectopic ureters or a neuropathic bladder.
Doppler ultrasound is able to investigate renal blood
flow; however, the interpretation of these findings
should be cautious, as vascular patterns may radically
change throughout gestation and after birth. However, it
seems that absent fetal renal arterial Doppler waveforms
on serial ultrasound of an abnormal fetal multicystic kid-
ney is correleted with renal nonfunction [10].
Biochemistry of fetal urine
The biochemical content of fetal urine may predict future
renal function. Urine electrolytes can be measured and
may reflect the fetal renal function [11–14]. High sodium
(>100 mEq/ml) and potassium (>90 mEq/ml) concentra-
tions, high osmolarity (>210 mosmol), an elevation of
β2-microglobulin [15] in fetal urine and low urine output
(<2 ml/h), associated with an echogenic or cystic ultra-
sound appearance of both kidneys with oligohydramnios,
are reported to be indicative of poor fetal renal function
[16]. More recently, urinary calcium was found to be sig-
nificantly higher in fetuses with renal dysplasia than
those with lower urinary tract obstruction and normal
clinical outcomes [17]. Urinary calcium and sodium are
the most-sensitive and specific predictors of dysplasia,
respectively.
The fetal kidney, placenta and fetal membranes are all
involved in fetal dialysis. The placenta and the fetal
membranes are likely to represent the main unit of dialy-
939
sis and the mother represents the system of reference.
This may explain two facts: (1) the newborn blood creat-
inine and the mother’s blood creatinine are usually iden-
tical; (2) anephric newborns have normal blood electro-
lytes at birth. It is therefore likely that the fetal kidney
has a poor qualitative control on the urine electrolytes, at
least during the first half of gestation. Both fetal glomer-
ular filtration and tubular function are likely to be poor.
Practical management of some common antenatally
diagnosed uropathies
The natural history of UFI located in the upper urinary
tract is now better understood from the numerous ran-
domised clinical studies that have compared conserva-
tive and surgical management of antenatally diagnosed
dilated upper tracts [18–21]. The degree of dilatation at
birth, however, does not consistently predict outcome,
and mild dilatation of the pelvis can deteriorate, suggest-
ing that long-term deterioration of antenatally diagnosed
UFI is a possibility [22–24]. Conversely, severely dilated
upper tracts may improve with time, confirming that an-
atomical criteria are poor prognostic indicators. Likewise
functional studies may improve or deteriorate with time,
regardless of the initial assessment. The following is an
outline of the management of some of the common post-
natal uropathies, which are summarised in Table 1.
Multicystic dysplastic kidney
Multicystic dysplastic kidneys are more commonly uni-
lateral, although bilateral cases have been reported. Asso-
ciated contralateral urological problems are frequently
encountered. Postnatally diagnosis is confirmed with an
ultrasound that shows multiple cysts, which have com-
pletely replaced the kidney (Fig. 1). Nuclear renograms
show a nonfunctioning kidney. Recently the management
of these patients has changed to a nonoperative approach.
These kidneys frequently involute, however size of the
kidney at initial presentation appears to predict involu-
tion, with few multicystic dysplastic kidneys greater than
6 cm involuting spontaneously. If the kidneys are not re-
solving many centres offer nephrectomy, as there have
been rare reports of hypertension and malignant change
associated with multicystic dysplastic kidneys [25].
Pyelo-ureteric junction anomalies
Fetal uropathies occur in 1 in 600–800 pregnancies and
pyelo-ureteric-junction (PUJ) anomalies are the com-
monest. There are three types of PUJ anomalies: extra-
mural, mural and intramural. Aberrant vessels mainly
cause extramural anomalies, although kinks, bands, ad-
hesions and arteriovenous malformation have also been
described, and these span the PUJ and reduce the urine
flow intermittently. In these cases, the dilatation of the
940
Table 1 Postnatal management of patients with an antenatally di- junction, PUV posteral urethral valves, DMSA dimercaptosuccinic
agnosed dilatation of the urinary tract (MCUG micturating cysto- acid, MAG 3 mercaptoacetyltriglycine, VUR vesico-ureteric re-
ureterography, PUJ pelvo-ureteric junction, VUJ vesico-ureteric flux)
Neonatal period
Ultrasound scan
MCUG
Antibiotics

6 weeks PUJ VUJ PUV VUR

MAG 3 scan MAG 3 scan MAG 3 scan DMSA scan
Ultrasound scan Ultrasound scan Valves resected at birth
Ultrasound scan

6 months Ultrasound scan Ultrasound scan Requires regular Ultrasound scan

MAG 3 scan MAG 3 scan follow-up by both DMSA
If stable observe If stable observe nephrologists and
If not operate If not stent ureter urologists

12 months Ultrasound scan Ultrasound scan Ultrasound scan

MAG 3 scan MAG 3 scan DMSA
If stable observe If stable observe
If not operate If not operate

Long-term Majority resolve Majority resolve If stable observe

Surgery only if Surgery only if If not operate
decrease in function decrease in function
symptomatic symptomatic

20 mm moderate and over 20 mm severe (Fig. 2). Ultra-

Fig. 1 Ultrasound of a multicystic dysplastic kidney
pelvis and symptoms are often intermittent. Mural anom-
alies are the most common and are due to an abnormal
distribution of the muscular and collagen fibres at the
level of the PUJ. Intramural anomalies are rare and are
mainly valve-like processes and benign fibroepithelial
polyps. Association between extramural and mural
anomalies are common, hence the difficulty in establish-
ing the exact cause of UFI.
Ultrasonography can measure the pelvic and calyceal
dilatation. Pelvic dilatation under 12 mm (anterio-poste-
rior diameter) is considered minimal, between 12 and
sonography can also show the echogenicity of the kidney
itself and the possible association of the PUJ anomaly
with other urological anomalies, such as a duplex
system, a horseshoe kidney or a ureterocele. Intravenous
urography (IVU) still remains a first-line investigation in
many centres. In the case of PUJ anomaly, it shows three
main signs: (1) a delayed excretion of contrast; (2) dis-
tended pelvis and calyces; (3) a delayed passage of con-
trast medium through the PUJ (>20 min). These signs are
mainly anatomical and are a poor indicator of renal func-
tion. Isotope renograms examine: (1) the perfusion of the
kidney (renal blood flow); (2) the relative function of
each kidney, which reflects the glomerular function (dur-
ing the first 30 s); (3) the parenchymal transit time of the
isotope; (4) the wash-out or clearance of the isotope
from the upper tract, which reflects the drainage (Fig. 3);
(5) finally, re-ascent of the radioactivity in the renal ar-
eas may be an indirect sign of vesico-ureteric reflux
(VUR) or, for other authors, a sign of true UFI revealed
by forced diuresis [26]. The drainage curves are depen-
dent on the degree of hydration of the child as well as
the function of the lower urinary tract. If they are normal
and if the relative function of the ipsilateral kidney is not
too low (>30%), there is no UFI. If they are abnormal,
they then suggest that there is a drainage problem, but
not necessarily at the PUJ level.
There are three commonly used radioisotopes: 99m
technetium-diethylenetriamine penta-acetic acid and

Fig. 2 Ultrasound showing a left pelvo-ureteric juncton obstruc-
tion, with dilated calyces and renal pelvis
Fig. 3 Mercaptoacetyltriglycine (MAG 3) renogram that shows
poor drainage in a left kidney with pelvo-ureteric junction obstruc-
tion compared with the normal right kidney
mercaptoacetyltriglycine (excreted by both glomerular
filtration and tubular secretion) both evaluate the relative
function and the drainage of the kidneys; 99m techne-
tium dimercaptosuccinic acid (DMSA) specifically lo-
calises in the proximal convoluted tubule and gives an
image of a functional renal mass.
There are four possible therapeutic approaches to PUJ
anomalies: (1) conservative management; (2) temporary
diversion of pelvic urine (percutaneous nephrostomy);
(3) surgical treatment; (4) fetal surgery / diversion, this is
still in the experimental stage and will not be discussed
further.
Conservative management of PUJ anomalies is justi-
fied in most infants. Three conditions are required to fol-
low a unilateral PUJ anomaly conservatively: (1) the
child must be asymptomatic; (2) the pelvic dilatation
should be either stable on repeated ultrasound scans or
should decrease; (3) the relative function on repeated
941
isotopic studies should be either stable or should im-
prove. Antibiotic prophylactic cover is recommended, al-
though no studies have formerly proven that it prevents
urinary tract infections.
Temporary diversion of the pelvic urine is indicated
in infants with severe unilateral pelvic dilatation and
poor relative function. The question is should this kidney
be repaired or removed? To answer the question, it is
necessary to place a percutaneous nephrostomy for 3–4
weeks, followed by reassessment of the relative function.
Either the function has improved and a pyeloplasty
should be performed, or the function remains poor and a
nephrectomy should be discussed.
Surgical treatment of the PUJ anomaly is advocated
by most urologists, in four principal circumstances: (1) a
symptomatic PUJ anomaly; (2) a declining function in
the dilated kidney; (3) an increasing pelvic dilatation; (4)
a bilateral moderate to severe dilatation of the pelvis.
These indications are not accepted by all: some operate
on infants during the 1st year of life, arguing that the
outcome of pyeloplasty is usually excellent in terms of
drainage and preserved renal function [22]. Conversely,
others will follow a conservative approach, even with an
increased pelvic dilatation [21]. When surgery is per-
formed, the most-common operation is a dismembered
pyeloplasty (Anderson-Hynes technique).
Vesico-ureteric junction anomalies
Many classifications of megaureter have been reported,
but practically there are two categories: (1) the megaure-
ters that are related to an abnormal vesico-ureteric junc-
tion (VUJ) (urine flow impairment or refluxing VUJ);
(2) the megaureters that are secondary to a dysfunction-
ing or obstructed lower urinary tract.
A megaureter may be due to a structural anomaly of
the distal segment of the ureter. Caused by collagen de-
position, cellular hypoplasia and muscular disarray, re-
gardless of the primary pathology a loss of functional
continuity results. Most studies have documented hyper-
plasia and hypertrophy of smooth muscle cells within the
942
Fig. 4 Ultrasound that shows a megaureter behind an empty blad-
der
walls of the dilated proximal ureter. These presumably
represent the ureter’s compensatory response to distal
UFI.
Anatomical studies include ultrasound scan of the uri-
nary tract (Fig. 4), IVU and micturating cystogram. All
three may show the degree and extent of urinary tract di-
latation, the micturating cystogram may also show the
presence of VUR. Distal anatomical obstruction of the
ureter and VUR may occur together. Functional studies
(diuresis renography) are useful to assess the degree of
functional UFI, however it is sometimes difficult to dis-
tinguish a PUJ from a VUJ anomaly which can occur to-
gether. In these difficult cases, an antegrade pyelogram
may be the only way to differentiate the two conditions.
Spontaneous improvement of ureteric dilatation is a
frequent event in megaureters, related to a faulty VUJ.
Resolution of UFI is common and conservative manage-
ment of megaureters is recommended when renal func-
tion and dilatation of the upper tract remain stable (or
improve), and when the child remains asymptomatic.
Antibiotic prophylaxis is recommended, especially in re-
fluxing megaureters. Regular isotope assessments are re-
quired to follow these children.
When the conservative approach fails, i.e. when
symptoms recur in spite of an adequate antibiotic pro-
phylactic cover or when renal function decreases on re-
peated isotope studies, or when dilatation of the urinary
tract increases, ureteric reimplantation is usually recom-
mended, except when renal function is poor (<15%),
then nephroureterectomy is indicated. The aim of the op-
eration is to excise the distal obstructive segment of the
ureter and reimplant the ureter.
Vesico-ureteric reflux
Previously reflux was diagnosed in patients being investi-
gated for urinary tract infections; however, with improve-
ments in antenatal scanning, dilatation secondary to reflux
can be identified during pregnancy. It accounts for ap-
proximately 10% of all antenatally diagnosed dilatation.
Over 90% of children with antenatally diagnosed reflux
are boys, this is in contrast to children with postnatally di-
agnosed reflux who are mainly girls [27–29]. This differ-
ence could be caused by transitory urethral obstruction
during the fetal development. Urodynamic observations in
male infants with VUR are supporting this theory [27].
When reflux has been identified it is important to pro-
ceed to a DMSA isotope scan so that individual renal
function and the presence of renal scarring can be as-
sessed. Approximately 60% of kidneys with reflux have
an abnormal renogram within the first 4 weeks of life, in
the majority this was before a urinary tract infection had
occurred. These data suggest that abnormalities in renal
development occur with reflux during intrauterine life.
Treatment of reflux diagnosed antenatally is by non-
operative means initially. All patients should be placed
on prophylactic antibiotics, in an attempt to avoid infec-
tion. Some authors suggest that circumcision can reduce
the number of urinary tract infections, this has not been
proven by a controlled trial, but is supported by consid-
erable anecdotal evidence [30]. When these methods fail
to prevent recurrent urinary tract infections or when
there is a significant decrease in renal function associat-
ed with scarring, then reimplantation of the refluxing
ureter is required to surgically correct the reflux.
Ureterocele
Ureteroceles are a cystic dilatation of the intravesical
portion of the ureter. They can cause UFI either to a sin-
gle system or more commonly to the upper pole of a du-
plex system. Investigations include: (1) ultrasonography
that can visualise both the ureterocele within the bladder
and the duplex kidney (Fig. 5); (2) IVU that is excellent
at identifying duplex kidneys and can identify uretero-
celes within the bladder; (3) micturating cystomethrogra-
phy, which excludes VUR both into the ipsilateral and
contralateral ureters; (4) finally an isotope scan should
be performed to assess the function of both moieties of
the duplex kidney.
There is considerable controversy over the manage-
ment of ureteroceles, which varies from simple endo-
scopic puncture of the ureterocele to upper pole hemine-
phrectomy and bladder reconstruction. Increasingly a
more-conservative approach is being adopted. In patients
who present in the neonatal period the first procedure is
endoscopic puncture: this was the only procedure re-
quired in 73% and resulted in drainage and preservation
of the upper pole in over 90% of patients [31]. In this
and other studies ureteric reflux was created in
20%–40% of patients and further surgery, including up-
per pole nephrectomy plus or minus bladder reconstruc-
tion, was required in 20%–80% of patients [31, 32].

Fig. 5 Ultrasound that shows a ureterocele (outlined by the cross-
es) in the bladder
Fig. 6 Micturating cystourethrogram which shows posterior ure-
thral valves distal to the dilated posterior urethra and prominent
bladder neck
Posterior urethral valves
Posterior urethral valves (PUV) are a congenital membrane
obstructing or partially obstructing the posterior urethra.
Rarely described in females, it is the most-common cause
of lower urinary obstruction in males. The incidence is be-
tween 1 in 4,000 and 1 in 25,000. Anatomical effects of
PUV on the urinary tract are dilatation and elongation of
the posterior urethra, the thickening of the bladder neck,
which can be wide open or very narrow, and the thickening
of the detrusor, which is often trabeculated. In addition to
the anatomical problems, bladder dysfunction is frequently
seen in association with PUV. VUR is often noticed, with a
marked dilatation of the upper tract and renal deterioration.
The thick bladder wall can cause a secondary UFI at the
level of the VUJ, and opening of the bladder (by doing a
vesicostomy or by augmenting the bladder) often relieves
vesico-ureteric obstruction. Some associated lesions of the
urinary tract, such as VUR (22%–70% of patients), bladder
diverticula and urine extravasation (with or without asci-
943
Table 2 Prenatal intervention forhydronephrosisa (UFI urine flow
impairment, Na sodium, Cl chloride)
Indications
Presumed significant UFI, persistent or progressive, bilateral
or in a solitary unit
Oligohydramnios
Otherwise healthy fetus without severe structural or karyotypic
abnormalities
Adequate fetal renal functional indices (urine output >2 ml/h, Na
<100 mmol/l, Cl <90 mmol/l, osmolality <210 mosmol/kg H2O)
Without overt renal dysplasia (minimal echogenicity, hydrone
phrosis proportional to lower tracts)
a From Blyth B, Duckett JW (1995) Neonatal obstructive uropathy.
In: Reed GB, Claireaux AE, Cockburn F (eds) Diseases of the fe-
tus and newborn. Chapman and Hall, London, p 1465
tes) can provide a pressure pop-off mechanism which min-
imises the renal consequences of PUV.
PUV should be suspected in a fetus with a thick-
walled bladder and bilateral dilatation of the upper uri-
nary tract, associated or not with renal dysplasia and oli-
gohydramnios. Oligohydramnios is usually noticed dur-
ing the second part of pregnancy, when most of the am-
niotic fluid is conveyed through the fetal urinary tract.
Despite modern ultrasonic equipment, only 16%–55% of
patients with PUV are detected before 24 weeks of ges-
tation.
Ultrasound scan of the urinary tract is the first-line in-
vestigation. It shows the dilatation of the upper urinary
tract, the possible abnormal echogenicity of the renal pa-
renchyma, the thick bladder wall associated or not with
bladder diverticula and the dilated posterior urethra. Peri-
neal ultrasound is increasingly able to detect urethral
anomalies. Micturating cystogram is still the gold stan-
dard investigation for detecting PUV (Fig. 6). Insertion of
a transurethral catheter can damage the anatomy of the
valve and some paediatric urologists prefer to perform su-
prapubic micturating cystograms. Isotope studies are also
essential to assess the renal consequences of PUV.
Antenatal treatment is rarely indicated, but may be
justified when oligohydramnios is deteriorating in a fetus
with bilateral dilatation of the upper urinary tract. Inser-
tion of a double-J stent between the fetal bladder or the
dilated kidneys and the amniotic cavity under ultrasound
guidance allows decompression of the urinary tract, pos-
sible preservation or development of the fetal kidney and
possible maturation of the fetal lungs by restoration of an
adequate volume of amniotic fluid. These antenatal di-
versions are usually performed quite late in pregnancy
and, once again, the benefit of such interventions in chil-
dren with PUV has not been yet demonstrated. Indica-
tions for possible in utero intervention are listed in Table 2.
After birth it is essential to resuscitate the child when
necessary, adequately drain the bladder and destroy the
valves. Resuscitation implies hydration, electrolyte re-
placement and antibiotics and should be performed in a
neonatal intensive care unit. Urine drainage can usually
be achieved either by inserting a transurethral or a supra-
pubic catheter. Occasionally a surgical vesicostomy is re-
944

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