SUA is common with many renal anomalies

associated genital anomalies:

female (40%): uterine, ovarian atrophy or agenesis

Male (10%): undescended testicle, testicular atrophy/agenesis

AFI = normal

Bladder = normal

absent kidney on one side

contralateral kidney = compensatory hypdertrophy (enlarged)

flattened "lying down" adrenal may be seen and occupy renal fossa.

good prognosis

AKA POTTER'S SYNDROME

AFI= severe oligo or anhydramnios

absent kidneys

lying down renals

bladder = nonvisualized

absent renal artery branches

Autosomal Recessive Polycystic Kidney Disease (infantile form

kidney contains microcysts; involves distal convoluted tubules & collecting ducts; cortex is spared

Prognosis: decreased renal functin; HTN; death at early age

bilateral, enlarged, echogenic kidneys

3-10 times normal renal size

enlarged AC

oligohydramnios

bladder may not be visualized

Multicystic Dysplastic Kidney Disease (Renal Dysplasia)

cystic lesions that correspond primarily to dilated collecting tubules. Cysts replace renal tissue measuring up to 6cm

usually unilateral, can be bi

prognosis: uni - excellent (more common)

bilat: fatal

uni: multiple smooth walled cysts of varying sizes

normal contralateral kidney

visible bladder, normal AFI

bilat: cysts bilaterally

absent bladder

oligohydramnios or anhydramnios

Autosomal Dominant Polycystic Kidney Disease (adult form)

on average shows up around 5th decade of life

unilat: RARELY unilateral

bilat: similar to ARPKD

symmetically enlarged kidneys

amniotic fluid may be normal 

visible bladder

normal kidneys in utero, f/u scans if family history

Occurs secondary to long standing obstruction in the 1st or early 2nd trimester

VACTERL

Prognosis: unilat - depends on renal function

bilat - poor prognosis

echogenic kidneys containing peripheral cortical cysts. variable #/sized of cysts

renal size can be small or enlarged

bilat: if caused by BOO and there is bilat hydro - thick wall bladder and severe oligo

assessment of renal cortex is important

obstruction at the junction between the renal pelvis and ureter

mos commone location for renal obstruction

most common cause of congenital urinary tract obstruction

most common in males

considered congenital hydronephrosis

usually unilateral

moderate to sever hydro

distended calyces with pelvis

enlarged kidney

unilat: non visualized ureter, visualized bladder, normal AFI

bilat: non visualized ureter or bladder, may have oligo

obstruction where the ureter dumps into bladder

hydro occurs secondary to obstruction

more common in males

may be unilat or bilat

affected kidney has dilatation of the pelvis and the ureters. ureter will appear hydroureter, megaureter; appears torturous

unilat: dilater ureter, normal bladder and AFI

bilat: both ureters dilated, small or nonvisual bladder, oligohydramnios

blockage at the base of the bladder that reduces or prevents the flow of urine into the urethra.

causes: urethral agenesis, urethral stricture, posterior urethral calves (most common cause)

mild to moderate hydro

dilated ureters

distended bladder

decreased AFI

marked dilatation of posterior urethra and bladder

sonographic sign = keyhole

bilateral hydro and dilated ureters

look at gender, if male its PUV. females cant have PUV

Autosomal recessive syndrome characterized by a TRIAD of findings: renal cystic dysplasia, posterior encephalocele (CNS abnormalities), polydactyly

associated findings: facial malformations, cardiac defects, increased AFP if encephalocele not covered by membrane

lethal

renal cystic dysplasia is most common

enlarged echogenic kidneys

enlarged AC

small or absent bladder

oligo is seen secondary to renal dysplasia, sometimes anhydramnios

grossly enlarged kidneys, 10-20 x normal size

congenital disorder or the urinary system

typically caused by mega cystitis (big bladder)

usually a result of PUV which leads to BOO

Characterized by classic TRIAD

urinary tract abnormalities

loss of abd musclulature due to megacystitis 

undescended testicles

enlarged kidneys, ureters, bladder

doughy abdomen

enlarged fluid filled renal pelvis and calyces

50% spontaneous

Most often bilateral  (R>L when unilat)

2% have downs

3% of normal fetuses have mild pelviectasis

Measurements for renal pelvis

Trans, AP

<24 wk: <4mm (recheck at 31 wk if >4mm)

24-30 weeks: <6mm (recheck when newborn is >6mm)

>30 wk: <8mm (recheck newborn if >8mm)

at 6 week check up: abnormal is >11mm