Fetal genitourinary

SONOGRAPHIC
APPEARANCE
 FETAL KIDNEYS:
 demonstrated at approximately 11 weeks transvaginally and
at 12 weeks using transabdominal probes.
 During the first trimester, the kidneys appear as hyper-echoic
oval structures at both sides of the spine
 This echogenicity will progressively decrease, and during the
third trimester, the cortical echogenicity will always be less
than that of the liver or spleen.
 Simultaneous to the decreased echogenicity, corticomedullary
(CMD) differentiation will appear at approximately 14 to 15
weeks.
 . Urine distending the renal pelvis may help in their
identification.

BLADDER
 Urine is first produced by the kidneys during the 9th
week of embryonic life.
 At this stage, the urine in the bladder can be
visualized as a fluid-filled structure within the fetal
pelvis.
 During the second and third trimester, the bladder will
empty and refill continuously every 25 to 30 minutes.
 The position of the fetal bladder can virtually always
be identified, because it lies between the umbilical
arteries within the fetal pelvis. These arteries are
readily seen with the use of color Doppler imaging.

URINARY TRACT
ABNORMALITIES
Systemic approach to assess
prenatal UT abnormalities include:
 Assessment of amniotic fluid index
 Localisation and characterisation of
urinary tract abnormalities
 Search for associated abnormalities

 Presence
 Number
 Position
 Appearance
 Unilateral or bilateral

BILATERAL
RENAL AGENESIS
 Ureteric buds fail to develop
 Lethal congenital anomaly
 1 in 4000 births and 2.5:1 male preponderance
 Associated with potter’s syndrome
 Pulmonary hypoplasia is the major cause of death

USG FINDINGS
 Severe oligohydraminos/anhydraminos
 Absent kidneys
 “LYING DOWN” adrenal sign
 Absent renal arteries on Color Doppler imaging
 Non visualisation of bladder (over 1 hour)

UNILATERAL
AGENESIS
 More common than B/L
 AFI, bladder- NORMAL
 Contralateral kidney shows compensatory
hypertrophy
 The ipsilateral adrenal gland is usually
present, and appears globular and should
not be mistaken for the kidney. Without the
adjacent kidney, the adrenal gland may be
elongated in appearance in what has been
called “the lying down adrenal sign”
 Contralateral kidney associated with
abnormalities ,most common—VUR

 One or both kidneys in abnormal position
 Pelvic kidney is the most common
 When ectopic kidney is located on opposite side of the abdomen
relative to its urethral insertion in to bladder is defined. CROSSED
FUSED ECTOPIA.
 Associated with abnormalities like VUR.

 Most common fusion anomaly
 On usg,
 Abnormal longitudinal axis of both
kidneys with bridge of renal tissue
connecting the lower poles
 Majority have anterior orientation of
pelvis B/L
 Associated with anomalies like turners
syndrome
 Higher prevalence of VUR, calculus ,UTI

Non – genetic cystic diseases
 Multi-cystic dysplastic kidney
(MCDK)
 Obstructive dysplasia
Genetic cystic diseases
 Autosomal recessive polycystic
kidney disease
 Autosomal dominant polycystic
kidney disease
RENAL CYSTIC DISEASE

 Most common renal cystic disease
 Kidney replaced by multiple cysts of varying sizes separated by dense
stromatolites and there is usually no renal parenchyma
 The cysts can be large, presenting as a large fetal abdominal mass, or on the
contrary, microcystic.

 Effect of urinary obstruction on subsequent renal development depends on the
time of onset and severity of obstruction
 Fetal urinary tract responds differently than adults to chronic obstruction by
possible development of macroscopic cysts
 Unilateral- UPJ OR UVJ obstruction
 Bilateral- Bladder outlet. Obstruction

AUTOSOMAL RECESSIVE
POLYCYSTIC KIDNEY
DISEASE
 ARPKD has an incidence of 1 in 20,000 live births and
often causes fetal and neonatal death.
 Renal failure and hepatic fibrosis develop in many
babies who survive the perinatal period
 The disease is characterised by marked elongation of
the collecting tubules that expand into multiple small
cysts. The cystic dilatation of the tubules is variable
and predominates in the medulla. The outer cortex is
spared because it contains no tubules. There is
associated biliary dysgenesis. Hepatic fibrosis has been
described on pathologic examination of affected
fetuses.
 The sonographic presentation varies according to the
severity of involvement. The most typical presentation
is that of markedly enlarged hyperechoic kidneys
without CMD).

 Another presentation of ARPKD can be reversed CMD with large kidneys.
 This finding is probably related to increased number of interfaces within the
medullae, and to inspissated material within the dilated tubules.
 It is an important observation because there are very few other causes of reversed
CMD.

AUTOSOMAL DOMINANT
POLYCYSTIC KIDNEY
DISEASE
 ADPKD is the most common form of polycystic
kidneys disease in humans , 1 in 800 live births.
 The disease is characterized by the presence of
multiple cysts that develop on the wall of collecting
tubules and nephrons. The cysts are scattered
within the cortex and medulla. These cysts enlarge
progressively and are typically identified in early
adulthood. Cysts may also develop in the liver,
spleen and pancreas in adults.

 Most commonly detected renal
abnormality
 Hydronephrosis refers to abnormal
dilatation of renal pelvis and calyces.
 Pyelectasis refers to milder form
with only dilatation of renal pelvis

 The severity of renal pelvic dilatation can be assessed using
different grading systems. Measuring the maximal antero-
posterior diameter of the renal pelvis (APPD) on a
transverse scan of the fetal abdomen is the generally
accepted method
 thresholds vary between 4 and 10 mm in the second
trimester, and between 7 and 10 mm in the third trimester.
Using a cut-off value of 4 mm in the second trimester,
results in a diagnosis of pyelectasis in 2% of pregnancies
(Adra et al., 1995; Corteville et al., 1991). A 7 mm cut-off in
the third trimester has a sensitivity of 100

 Obstruction at the UPJ is the most common cause of
non-physiologic neonatal hydronephrosis,
 It is also one of the most common reasons for postnatal
surgery of the UT.
 Most cases of UPJ obstruction are functional (caused by
a muscular abnormality) rather than the result of mixed
anatomic lesions such as fibrous adhesions, kinks,
valves, or aberrant vessels.
 On sonography, a dilated renal pelvis with or without
caliectasis is identified. he ureter and the bladder are
not dilated. Severe chronic obstruction leads to
effacement of the calyces and thinning of the renal
cortex (SFU grade 4)

 More common in males
 Primary megaureters- 3 types

LOWER URINARY
TRACT
OBSTRUCTION
 Fetal megacystis:
 10-14 weeks
 Longitudinal diameter of bladder- >7mm or
more
 2nd- 3rd trimester – enlarged bladder ,fails to
empty over 45 min of observation
 If >7-15mm mostly associated with
chromosomal abnormalities.

CAUSES OF
FETAL
MEGACYSTI
S
 Posterior urethral valve
 Urethral atresia or stricture
 Ureterocole
 Prune belly syndrome
 Megalourethra
 Cloacal malformation
 Megacystis microcolon intestinal
hypoperistalisis syndrome

 Most common cause
 Seen exclusively in males
 Infra vesicular pressure generated secondary to obstruction results in persistently
dilated UB with a dilated proximal dilated urethra giving KEY HOLE appearance
 Thickening of bladder wall,B/L tortuous hydroureters and hydronephrosis

 most severe, and earliest detected, form of
obstructive uropathy. he sonographic features
include a greatly distended bladder that may
ill the whole abdomen, and anhydramnios
after the first trimester
 . Urethral atresia is almost always fatal,
because of associated renal dysplasia and
pulmonary hypoplasia, and only case reports
of survivors following antenatal treatment
have been described.195,1

 characterized by a congenital deficiency of the
mesodermal tissues of the phallus, with dilation of the
penile urethra and enlargement of the penis.
 this condition has been classified into two types,
fusiform and scaphoid urethra, but it is preferable to
consider it as a spectrum.
 Urinary stasis in the dilated penile urethra results in
functional obstruction of the UT.
 The prenatal sonographic findings include those of
LUTO, with dilation and elongation of the penile
urethra
 . Associated malformations of the UT include urethral
atresia, posterior urethral valves, prune belly syndrome,
and horseshoe kidney. Abnormalities involving the GI
tract and spine and VACTERL association on have been
reported

 Deficiency of abdominal musculature and cryptorchidism
 Rarely in females
 Bladder is large thin walled

 PRESENCE
 APPEARANCE AND SIZE

FAILURE OF URINE
PRODUCTION
 Bilateral severe renal abnormalities
like renal agenesis, MCDK, ARPKD,
UPJ obstruction.
 Severe intrauterine growth restriction
or placental insufficiency
FAILURE TO STORE URINE
 Bladder exstrophy
 Cloacal exstrophy
 Cloacal malformation
 Bilateral ectopic ureter with drainage
outside of bladder

 Incomplete median closure of the inferior part
of the anterior abdominal wall and anterior
wall of urinary bladder
 On USG,
 AFI and kidneys are normal but bladder is not
identified
 Irregular mass may be seen arising from the
anterior abdominal wall inferior to umbilicus
 Low umbilical cord insertion
 Widening of pubic bones
 Rarely reported with OEIS complex
Longitudinal scan of the lower fetal abdomen in a 29-
week fetus shows an irregular mass on the anterior
abdominal wall (arrows), below the umbilical cord
insertion (U). A luid-illed bladder was not identiied.
Note normal amniotic luid volume. (B) Corresponding
photograph shows the exposed bladder (arrows) below
the umbilical cord (U).

 More than half of all congenital abdominal masses
found in the neonate originate in the kidney.
 In the fetus, the most common renal tumor is the
mesoblastic nephroma .
 It appears as a solid tumor that is sometimes difficult
to delineate from the adjacent renal parenchyma.
 The tumor can appear partially cystic.
 In utero, polyhydramnios is typically associated and
hypertension develops after birth.
 Cases of fetal renal Wilms’ tumor have been reported
as solid or partially cystic tumors. The prognosis is
good. Bilateral involvement suggests
nephroblastomatosis, which is a condition with
multiple benign nodular lesions.

 Whenever a mass is detected in the suprarenal
area, a neuroblastoma should be suspected first
regardless of the pattern of the mass
 Neuroblastoma may present as a cystic, a solid
or more complex appearance.
 Color Doppler imaging may demonstrate
increasing vascularization of the hyperechogenic
regions of the mass.
 The differential diagnosis should include adrenal
hemorrhage, associated or not with RVT, and
adrenal cysts.
 . Extra-adrenal causes, such as sub-
diaphragmatic pulmonary sequestration, should
also be included in the differential diagnosis

Fetal genitourinary

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