BJOG: an International Journal of Obstetrics and Gynaecology
December 2002, Vol. 109, pp. 1388 –1393
Prenatal diagnosis of bilateral isolated fetal hyperechogenic
kidneys. Is it possible to predict long term outcome?
V. Tsatsarisa,b, M.F. Gagnadouxb,c, M.C. Aubryb,d, M.C. Gublerb,e,
Y. Dumezb,d, M. Dommerguesb,d,*
Objective To study perinatal and long term outcome following prenatal diagnosis of hyperechogenic
kidneys.
Design Prospective observational cohort study.
Setting The Maternité Port-Royal Hôpital Cochin and at the Departments of Obstetrics and Paediatric
Nephrology, Necker Enfants Malades in Paris, France.
Population Forty-three fetuses with isolated bilateral hyperechogenic kidneys.
Methods All patients referred with isolated bilateral hyperechogenic fetal kidneys were followed up
prospectively up to 34 –132 months. The following prenatal items were analysed: fetal kidney size,
amniotic fluid volume, gestational age at diagnosis, family history and renal ultrasound in parents.
Postmortem examination was carried out in cases with perinatal death. Postnatal follow up of survivors
included postnatal ultrasound, blood pressure, serum creatinine, proteinuria, need for restricted diet, weight
and height and renal biopsy when available.
Main outcome measures Aetiology of hyperechogenicity, perinatal mortality and renal function in survivors.
Results The aetiology could be established by family history, postmortem or postnatal data, but not by
prenatal ultrasound. There were 20 autosomal recessive, 8 autosomal dominant polycystic kidney
diseases, 9 other renal disorders and 6 symptom-free survivors without aetiological diagnosis. There
were 19 terminations of pregnancy, 5 neonatal deaths and 19 survivors, of whom 14 had normal renal
function three had mild and two had end stage renal failure. None of those with severe oligohydramnios and fetal kidneys > 4 SD survived (n ¼ 14, 10 terminations and 4 neonatal deaths),
whereas of the 17 with normal amniotic fluid volume and kidneys < 4 SD, 14 survived, of whom 9 were
symptom-free.
Conclusion Aetiology could not be established prenatally in the absence of familial data. Kidney size and
amniotic fluid volume were the best prenatal predictors of outcome.
INTRODUCTION
Obstetricians are increasingly facing the challenge of
counselling pregnant women following sonographic prenatal
diagnosis of fetal abnormalities carrying an uncertain
prognosis. Prenatal diagnosis of hyperechogenic kidneys
a
Department of Obstetrics, Maternité Port-Royal Hôpital
Cochin, AP-HP, Paris, France
b
Université Paris V, Paris, France
c
Department of Paediatric Nephrology, Hôpital Necker
Enfants Malades, AP-HP, Paris, France
d
Department of Obstetrics, Hôpital Necker Enfants
Malades, AP-HP, Paris, France
e
INSERM U423, Hôpital Necker Enfants Malades, AP-HP,
Paris, France
* Correspondence: Dr M. Dommergues, Maternité Hôpital Necker, 149
Rue de Sèvres, 75015 Paris, France.
D RCOG 2002 BJOG: an International Journal of Obstetrics and Gynaecology
PII: S 1 4 7 0 - 0 3 2 8 ( 0 2 ) 0 2 9 5 5 - 5
is an example of this difficult situation, in which providing
women with over pessimistic information leads to unnecessary termination of pregnancy, whereas reassuring patients
without any restriction may be unfair. This underscores
the need for basing prenatal counselling on prenatal cohorts
with a long term postnatal follow up. There are few series
of prenatal diagnosis with postnatal follow up1 – 5, and
performing prenatal counselling based only on postnatal
data is flawed by a number of biases. First, fetal sonography usually fails to provide an accurate aetiological
diagnosis, and fetal hyperechogenic kidneys may result
from a variety of aetiologies. Second, within each aetiological group, there is a wide range of outcomes. Postnatal
series are likely to overlook the most severe cases, leading
to perinatal death, as well as the mildest ones, which may
remain undetectable clinically over a long period. So far,
the outcome of fetal hyperechogenic kidneys can only
be predicted accurately in the most severe cases, in which
terminal renal failure is ascertained by severe oligohydramnios. In order to provide data on the long term outcome of
fetal hyperechogenic kidneys, we conducted a prospective
www.bjog-elsevier.com
LONG TERM POSTNATAL FOLLOW-UP OF BILATERAL ISOLATED FETAL HYPERECHOGENIC KIDNEYS
A
1389
B
L
L
K
K
C
K
L
Fig. 1. Legend: K ¼ kidney; L ¼ liver; A ¼ hyperechogenic kidney; B ¼ borderline kidney, yet considered as hyperechogenic; C ¼ non-hyperechogenic
kidney.
cohort study on 45 cases with prenatal diagnosis of hyperechogenic kidneys.
METHODS
Between 1985 and 1996, the diagnosis of isolated bilateral hyperechogenic fetal kidneys was made in 45 pregnant
women referred to our department. Eleven patients had
been screened for fetal kidneys abnormalities because of a
family history of autosomal recessive (n ¼ 4) or dominant
(n ¼ 7) polycystic kidney disease. In 34 cases, abnormal
fetal kidneys were picked up by routine ultrasound.
Additional anomalies were ruled out based on ultrasound
and fetal karyotyping. Absence of associated anomalies
was confirmed by postnatal or by postmortem examination.
Cases with (i) urinary tract dilatation, (ii) macrocysts
suggestive of multicystic kidneys or (iii) extra urinary
abnormalities were not included.
D RCOG 2002 Br J Obstet Gynaecol 109, pp. 1388 – 1393
Kidneys were considered as hyperechogenic when their
echogenicity was greater than that of the liver (Fig. 1). The
size of the kidneys was expressed as standard deviations
above or below the mean derived from the growth charts of
Le Guern et al.6.
The amount of amniotic fluid was assessed in a semiquantitative fashion. Oligohydramnios was considered as
severe when no amniotic pool greater than 2 cm could be
identified by ultrasound. The diagnosis of moderate oligohydramnios was made on a subjective basis7.
In the absence of a positive family history, parents
were screened by ultrasound for renal cysts suggestive of
autosomal dominant polycystic kidney disease (ADPKD).
Prenatal management was based on the assessment of
amniotic fluid volume. Termination of pregnancy was
offered in cases with severe oligohydramnios. In cases with
moderate oligohydramnios, the decision to continue the
pregnancy or not was postponed and was eventually made
based on prenatal sonographic follow up. In cases with
1390
V. TSATSARIS ET AL.
Table 1. Autosomal recessive polycystic kidney disease.
Case
GA
AF
Perinatal
outcome
Indication for
ultrasound
Kidney’s
height (SD)
Follow up
(months)
Creatinine
clearance
Clinical symptoms
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
29
22
18
27
32
24
35
30
34
30
31
28
36
33
21
29
34
32
35
27
MOH
N
N
MOH
SOH
SOH
SOH
SOH
SOH
SOH
SOH
MOH
MOH
SOH
N
MOH
N
N
N
N
TOP
TOP
TOP
TOP
TOP
TOP
TOP
TOP
TOP
TOP
NND
NND
NND
NND
alive
alive
alive
alive
alive
alive
family history
family history
family history
routine
routine
routine
routine
routine
routine
routine
family history
routine
routine
routine
family history
routine
routine
routine
routine
routine
3
2
3
3
7
3
4
4
8
6
4
9
9
7
3
3
3.5
–
5
1.8
132
132
84
84
120
120
49
121
96
55
159
106
hypertension, renal failure
hypertension
hypertension
renal failure
none
none
Postnatal ultrasound
large HE kidneys and
large HE kidneys and
large HE kidneys and
HE kidneys and cysts
large HE kidneys and
multiple microcysts
cysts
cysts
cysts
cysts
TOP ¼ termination of pregnancy; AF ¼ amniotic fluid volume (MOH ¼ moderate oligohydramnios, PH ¼ polyhydramnios, SOH ¼ severe oligohydramnios,
N ¼ normal amniotic fluid volume); NND ¼ neonatal death; HE kidneys ¼ hyperechogenic kidneys; GA ¼ gestational age at diagnosis. Creatinine clearance
was calculated according to Schwartz formula (mL/min/1.73 m2).
normal amniotic fluid volume, parents were encouraged to
continue the pregnancy. However, following counselling by
a fetal medicine specialist and a paediatric nephrologist,
parental autonomy was respected as for continuing or
terminating the pregnancy.
Postmortem histological examination was performed in
all cases of termination of pregnancy or of neonatal death.
Among survivors, postnatal follow up was obtained
based on reviewing medical records of children followed
in our institution or interviewing the paediatrician in charge
of children followed outside our hospital. The following
items were recorded: (1) postnatal ultrasound, (2) blood
pressure, (3) serum creatinine, (4) proteinuria, (5) need for
restricted diet, (6) weight and height and (8) renal biopsy
when available. Creatinine clearance was calculated according to Schwartz formula8. We did not screen for PKD1 or
PKD2 gene mutations routinely because of technical limitations related to the genetic and allelic heterogeneity of
ADPKD and to the complex structure of PKD genes.
RESULTS
Of 45 cases in which isolated hyperechogenic kidneys
were diagnosed in utero, 43 had a complete follow up
and form our database. There were 19 terminations of
Table 2. Autosomal dominant polycystic kidney disease.
Case
GA
AF
Perinatal
outcome
Indication for
ultrasound
Kidney’s
height (SD)
Follow up
(months)
Creatinine
clearance
Clinical symptoms
Postnatal ultrasound
21
22
23
24
25
26
27
28
21
24
23
33
23
36
28
24
MOH
SOH
SOH
N
N
N
MOH
N
TOP
TOP
TOP
alive
alive
alive
alive
alive
routine
routine
family history
family history
family history
family history
routine
routine
8
9
7
2
2
5.5
1
2
58
88
130
36
34
NA
NA
72
90
97
none
none
hypertension, renal failure
none
none
NA
NA
large HE kidneys and cysts
HE kidneys and cysts
HE kidneys and cysts
TOP ¼ termination of pregnancy; AF ¼ amniotic fluid volume (MOH ¼ moderate oligohydramnios, PH ¼ polyhydramnios, SOH ¼ severe oligohydramnios,
N ¼ normal amniotic fluid volume); GA ¼ gestational age at diagnosis; NA ¼ not available. Creatinine clearance was calculated according to Schwartz
formula (mL/min/1.73 m2).
Cases 24 and 25 were two sisters born to a mother affected by ADPKD who elected not to have any imaging or biochemical screening performed in her
children. In cases in which fetal renal hyperechogenicity was picked up by routine ultrasound, the diagnosis of ADPKD was made based on renal cysts in one
of the parents or grandparents.
D RCOG 2002 Br J Obstet Gynaecol 109, pp. 1388 – 1393
LONG TERM POSTNATAL FOLLOW-UP OF BILATERAL ISOLATED FETAL HYPERECHOGENIC KIDNEYS
1391
Table 3. Other renal abnormalities.
Case
GA
AF
Perinatal
outcome
Indication for
ultrasound
Kidney
height SD
Follow up
(months)
Creatinine
clearance
29
30
31
32
33
34
35
36
34
23
21
22
31
23
20
30
SOH
SOH
N
MOH
SOH
N
SOH
PH
TOP
TOP
TOP
TOP
TOP
TOP
NND
alive
routine
routine
routine
routine
routine
routine
routine
routine
2.5
1
5
4
6
1.5
1
1
60
74
37
22
N
alive
routine
3.5
61
11
Clinical symptoms/
postmortem diagnosis
diffuse cortical cysts
multicystic horseshoe kidney
cystic dysplasia
cystic dysplasia
multicystic kidney
nephrocalcinosis
tubular dysgenesis
MRF
CTI, ESRF, hypertension,
renal transplantation graft rejection
Postnatal ultrasound
small hyperechogenic
kidneys with cysts
cortical microcysts
TOP ¼ termination of pregnancy; AF ¼ amniotic fluid volume (MOH ¼ moderate oligohydramnios, PH ¼ polyhydramnios, SOH ¼ severe oligohydramnios,
N ¼ normal); CMD ¼ corticomedulary differentiation; GA ¼ gestational age at diagnosis; MRF ¼ moderate renal failure; NND ¼ neonatal death; ESRF ¼
end stage renal failure; CTI ¼ chronic tubulointerstitial nephropathy with cortical microcysts. Creatinine clearance was calculated according to Schwartz
formula (mL/min/1.73 m2).
pregnancy, 5 neonatal deaths and 19 survivors, who were
followed for 34 –132 months (median: 84 months). Sonographic data such as kidney size, amniotic fluid volume or
the degree of hyperechogenicity did not contribute to
establishing the aetiology. This was achieved by postmortem results, postnatal follow up, and/or family history either
known before pregnancy or uncovered following prenatal
diagnosis. Twenty cases (46%) were diagnosed as autosomal recessive polycystic kidney disease (ARPKD) eight
(19%) as ADPKD and nine (21%) as other renal disorders.
In the remaining six cases (14%), it was not possible to
establish the aetiology of fetal renal hyperechogenicity.
Of the 34 cases in which hyperechogenic fetal kidneys
were picked up by routine sonography in the absence of
a known family history, there were 15 ARPKD (44%),
4 ADPKD (12%), 9 cases with other renal disorders (26%)
and 6 idiopathic cases (18%).
Of the 20 cases of ARPKD, 15 were picked up by
routine sonographic screening, whereas in 5 cases prenatal
sonography was performed because of a family history
(Table 1). At the time of referral, oligohydramnios was
severe in eight cases, moderate in five and with normal
amniotic fluid volume in seven cases. There were 10 terminations of pregnancy, 4 neonatal deaths and 6 children
survived. Of the survivors, two were symptom-free, three
had hypertension with renal insufficiency in one of them
and one had renal failure.
The diagnosis of ADPKD was made in eight cases
(Table 2). In four cases, prenatal sonography had been
performed because of a family history. In the other four
cases, hyperechogenic kidneys were picked up by routine
sonographic screening and the diagnosis of ADPKD was
ascertained because renal cysts were found in parents or
grandparents. Oligohydramnios was severe in two cases,
moderate in two, and with normal amniotic fluid volume
in four cases. There were three terminations of pregnancy
and no neonatal death. Four out of five survivors were
symptom-free. One had moderate renal insufficiency with
systemic hypertension.
Nine infants were eventually considered to have another
nephropathy (Table 3). The diagnosis was based on
histological examination in eight cases and on postnatal
Table 4. Cases with hyperechogenic kidneys without precise diagnosis: prenatal data and postnatal follow up.
Case
GA
AF
Perinatal
outcome
Indication for
ultrasound
Kidney
height SD
Follow up
(months)
Creatinine
clearance
Clinical symptoms
Postnatal ultrasound
38
39
40
41
42
43
33
27
24
32
30
37
N
N
N
N
PH
N
alive
alive
alive
alive
alive
alive
routine
routine
routine
routine
routine
routine
0
1
2
3.1
3
3.5
96
100
72
130
130
67
136
87
125
105
147
97
no
diabetes
no
no
no
no
normal*
normal*
normal*
normal*
abnormal**
abnormal***
AF ¼ amniotic fluid volume (PH ¼ polyhydramnios, N ¼ normal), GA ¼ gestational age at diagnosis, NN ¼ neonatal. Creatinine clearance was calculated
with Schwartz formula (mL/min/1.73 m2).
* Transient hyperechogenic kidneys. Hyperechogenicity was confirmed in the neonatal period, but resolved at subsequent follow up.
** Two cysts measuring 10 mm in diameter in each kidney.
*** Moderately hyperechogenic kidneys.
D RCOG 2002 Br J Obstet Gynaecol 109, pp. 1388 – 1393
1392
V. TSATSARIS ET AL.
Table 5. Sonographic features and outcome.
Oligohydramnios* (n ¼ 22)
Normal or increased amniotic volume (n ¼ 21)
Kidney height 4 SD above the mean (n ¼ 17)
Kidney height < 4 SD above the mean (n ¼ 25)
Oligohydramnios and kidney height 4 SD above the mean (n ¼ 14)
Normal or increased amniotic volume and
kidney height < 4 SD above the mean (n ¼ 17)
Termination
of pregnancy
Neonatal death
Survivors
Symptom-free
survivors
15
4
11
8
10
3
5
0
4
1
4
0
2
17
2
16
0
14
1
11
1
10
0
9
* Moderate or severe at the time of prenatal diagnosis.
ultrasonography in one. At the time of referral, oligohydramnios was severe in four cases, moderate in one, with
normal amniotic fluid volume in three cases and with was
polyhydramnios in one case.
There were six terminations of pregnancy and one
neonatal death. Of the two survivors, one developed end
stage renal failure and underwent renal transplantation at
the age of five. The other one had mild renal failure at
six years, with small hyperechogenic kidneys (hypoplastic
kidneys).
In six children, it was not possible to obtain a precise
diagnosis despite careful postnatal evaluation (Table 4).
There was no case with oligohydramnios. In every case,
neonatal ultrasonography confirmed renal hyperechogenicity, but in four children, renal sonography turned normal at
subsequent follow up. Of the four children with transient
hyperechogenicity, three remained symptom free and one
had diabetes mellitus at the age of 11 months and minor
learning disability at eight years. Both children with
persistent unexplained renal hyperechogenicity remained
symptom free.
Overall, amniotic fluid volume and kidney size correlated
with outcome (Table 5). There were no survivors among
fetuses with kidneys larger than 4 SD above the mean for
gestational age and oligohydramnios at the time of diagnosis. Most fetuses with normal amniotic fluid volume and
kidneys smaller than 4 SD above the mean survived, the
majority of which became symptom-free children.
DISCUSSION
Our results provide information on the spectrum of renal
disorders associated with isolated fetal hyperechogenic
kidneys. Prenatal diagnosis of hyperechogenic kidneys
may be beneficial to infants, by allowing early recognition
and treatment of a renal disease. However, prenatal identification of a fetal renal abnormality may be extremely
stressful for the parents and can even be devastating when
termination of pregnancy is sought because long term
outcome appears uncertain. This prompted us to follow
up prospectively all infants referred to our unit because of
isolated fetal hyperechogenic kidneys.
Increased echogenicity of the renal parenchyma is nonspecific and occurs as a response to different changes in
renal tissue1. Interstitial infiltration, sclerosis and multiple
microscopic cortical and medullary cysts may account for
hyperechogenicity even in the absence of macrocysts1,9.
ARPKD, ADPKD and dysplasia are the most common
causes for fetal renal hyperechogenicity. However, it is
not possible to ascertain the aetiology of fetal hyperechogenic kidneys by ultrasound alone10. The only prospective
survey of hyperechogenic fetal kidneys published so far
consisted of 19 cases, 14 of which had bilateral increased
renal parenchymal echogenicity. Of the latter, there were
four with ARPKD, three multicystic kidneys, two hydronephrosis, one renal dysplasia and four ‘false positive’1. In
our experience, ARPKD was the leading, but not the sole
cause of fetal hyperechogenicity. ADPKD was not uncommon. We were not able to discriminate ARPKD from
ADPKD based on prenatal ultrasound. The incidence of
ADPKD may have been under-estimated in our study, since
the diagnosis can be overlooked in survivors without a
family history. Cases with other renal disorders constitute a
heterogeneous group. Most of the time, the diagnosis was
based on histological findings following termination of
pregnancy for severe oligohydramnios and abnormal kidneys. Our most striking finding is that a substantial number
of children survived without symptoms and could not be
allocated to a precise aetiological group. This reflects the
recruitment bias inherent to prenatal screening, which
uncovers morphological abnormalities that do not necessarily cause symptoms. It is possible that these children will
never develop any disease, which could correspond to the
postnatal entity referred to as ‘transient nephromegaly’11 or
medullary hyperechogenicity12. Further follow up might
also uncover a renal condition later in childhood or even in
adulthood, such as ADPKD.
At the other end of the spectrum of outcomes were
fetuses with severe oligohydramnios, due to anuria and
end stage renal failure. Short term outcome was then
uniformly poor, regardless of the aetiology. However, these
results are biased by the high rate of pregnancy terminations
in cases with oligohydramnios. Nevertheless, the three
pregnancies that were continued despite oligohydramnios
resulted in neonatal death, supporting the concept that
D RCOG 2002 Br J Obstet Gynaecol 109, pp. 1388 – 1393
LONG TERM POSTNATAL FOLLOW-UP OF BILATERAL ISOLATED FETAL HYPERECHOGENIC KIDNEYS
severe oligohydramnios complicating a fetal nephropathy
is an ominous finding. Severe oligohydramnios was documented both in ARPKD and ADPKD, confirming the
variability of expression of these conditions13.
Apart from these obviously severe cases, it is difficult to
predict the long term postnatal outcome of fetuses with renal
hyperechogenicity. However, this question is central for
couples seeking advice following prenatal diagnosis. So far,
prenatal studies focussed in predicting short term outcome2.
Because series of renal diseases diagnosed in neonates could
be biased towards the most severe cases, we choose to
follow up a cohort of patients in whom diagnosis was made
prenatally. A relatively long follow up was also required to
obviate the most common limit of prenatal studies with a
short term follow up, which is to overdiagnose cases as
‘idiopathic’ and to overlook morbidity in infancy. In our
cohort, outcomes of children with documented ARPKD or
ADPKD were consistent with what would be expected from
paediatric series with neonatal diagnosis 5,14,15. However,
the proportion of ‘idiopathic’ symptom-free survivors must
be kept in mind while counselling parents after prenatal
diagnosis of hyperechogenic kidneys.
We are currently investigating the potential role of fetal
urinalysis or fetal blood sampling to predict long term
paediatric outcome or fetal nephropathies, but so far this
question cannot be addressed based on currently available
literature.
In conclusion, our results suggest that prenatal counselling following the diagnosis of isolated bilateral hyperechogenic kidneys should emphasise that establishing the
aetiology is difficult, except when renal cysts are found in
one of the parents. While patients with very large kidneys
and severe oligohydramnios are likely to have a poor
outcome, the chances to survive without significant morbidity in infancy are high when amniotic fluid volume remains
normal and when the kidneys are moderately enlarged.
Acknowledgements
The authors would like to thank all the doctors who
provided them with postnatal follow up.
D RCOG 2002 Br J Obstet Gynaecol 109, pp. 1388 – 1393
1393
References
1. Estroff JA, Mandell J, Benacerraf BR. Increased renal parenchymal
echogenicity in the fetus: importance and clinical outcome. Radiology
1991;181:135 – 139.
2. Carr MC, Benacerraf BR, Estroff JA, Mandell J. Prenatally diagnosed bilateral hyperechoic kidneys with normal amniotic fluid: postnatal outcome. J Urol 1995;153:442 – 444.
3. Fick GM, Johnson AM, Strain JD, et al. Characteristics of very early
onset autosomal dominant polycystic kidney disease. J Am Soc
Nephrol 1993;3:1863 – 1870.
4. Romero R, Cullen M, Jeanty P, et al. The diagnosis of congenital
renal anomalies with ultrasound: II. Infantile polycystic kidney
disease. Am J Obstet Gynecol 1984;150:259 – 262.
5. Blickman JG, Bramson RT, Herrin JT. Autosomal recessive polycystic kidney disease: long-term sonographic findings in patients surviving the neonatal period. Am J Roentgenol 1995;164:1247 – 1250.
6. Le Guern H, Collet M, Jehannin B, Boog G. Le rein foetal, pathologie, sémiologie échographique et corrélations pré et post-natales.
JEMU 1983;4:65 – 71.
7. Chamberlain PF, Manning FA, Morrison I, Harman CR, Lange IR.
Ultrasound evaluation of amniotic fluid volume: I. The relationship
of marginal and decreased amniotic fluid volumes to perinatal outcome. Am J Obstet Gynecol 1984;150:245 – 249.
8. Schwartz GL. A simple estimate of glomerular filtration rate in children derived from body length and plasma creatinine. Pediatrics 1976;
58:259 – 263.
9. Guay-Woodford LM, Galliani CA, Musulman-Mroczek E, Spear GS,
Guillot AP, Bernstein J. Diffuse renal cystic disease in children:
morphologic and genetic correlations. Pediatr Nephrol 1998;12:
173 – 182.
10. Chitty LS, Clark T, Maxwell D. Perlman syndrome — a cause of
enlarged, hyperechogenic kidneys. Prenat Diagn 1998;18:1163 – 1168.
11. Stapleton FB, Hilton S, Wilcox J, Leopold GR. Transient nephromegaly simulating infantile polycystic disease of the kidneys. Pediatrics
1981;67:554 – 559.
12. Howlett DC, Greenwood KL, Jarosz JM, MacDonald LM, Saunders
AJ. The incidence of transient renal medullary hyperechogenicity in
neonatal ultrasound examination. Br J Radiol 1997;70:140 – 143.
13. Lilford RJ, Irving HC, Allibone EB. A tale of two prior probabilities — avoiding the false positive antenatal diagnosis of autosomal
recessive polycystic kidney disease. Br J Obstet Gynaecol 1992;99:
216 – 219.
14. Fick GM, Duley IT, Johnson AM, Strain JD, Manco-Johnson ML,
Gabow PA. The spectrum of autosomal dominant polycystic kidney
disease in children. J Am Soc Nephrol 1994;4:1654 – 1660.
15. Fick GM, Gabow PA. Natural history of autosomal dominant polycystic kidney disease. Annu Rev Med 1994;45:23 – 29.
Accepted 4 September 2002