Most cases of mild isolated unilateral or bilateral hydronephrosis on prenatal US ultimately resolve [4,32,33]. The incidence of transient hydronephrosis is between 41% and 88% [6,34,35]. The etiology of transient hydronephrosis is still elusive, but it appears that immature and poorly coordinated peristalsis of the smooth muscle of the renal pelvis leads to inadequate emptying and resultant urinary stasis within the renal pelvis [28]. The timing of resolution varies considerably, but it usually occurs during the first few years of life [4]. Earlier resolution is expected for milder grades of hydronephrosis, with most cases of SFU grade 1 to 2 hydronephrosis resolving by 18 months of age [6]. The differentiation of transient hydronephrosis from true ureteropelvic junction obstruction is virtually impossible with a single US examination, and serial follow-up with US is recommended until resolution (Fig. 2) [4,10].

Ureteropelvic junction obstruction is defined as the functional or anatomic obstruction of urine flow at the ureteropelvic junction. Ureteropelvic junction obstruction is the most common cause of obstructive hydronephrosis in neonates and shows a male and left-side predominance [2,36]. Ureteropelvic junction obstruction can be caused by abnormally developed ureteral smooth muscle at the ureteropelvic junction, resulting in an aperistaltic segment. Other intrinsic (intrinsic stenosis, valve or folds, fibrous bands) and extrinsic (abnormal vessels crossing the upper ureter or renal pelvis) factors have also been implicated as causes of ureteropelvic junction obstruction [37]. Ultrasonographic findings of ureteropelvic junction obstruction follow the general rule of obstruction: dilation of the upstream structure and collapse of the downstream structure beyond the transition point. US of the involved kidney shows multiple dilated calyces of uniform size that communicate with a dilated renal pelvis with abrupt narrowing at the level of the ureteropelvic junction in the absence of dilated ureter on a scan through the bladder (Fig. 3) [3]. In more severe cases, the renal parenchyma gets thinner. Cases of severe in utero obstruction may be accompanied by findings including renal dysplasia, subcapsular urinoma, and urine ascites. Sonographic features of renal dysplasia include increased parenchymal echogenicity, loss of corticomedullary differentiation, and the advent of cortical cysts (Fig. 4) [38].

Megaureter is a descriptive term referring to a dilated ureter [3,39]. This condition can be induced by various factors. Any abnormalities involving the distal ureter, bladder, or urethra, including congenital distal ureteral stricture, distal ureteral valve, ureterocele, neurogenic bladder, bladder outlet obstruction, posterior urethral valve, calculi, blood clot, or polyp, can lead to dilation of the ureter. Primary megaureter refers to ureteral dilation without an identifiable anatomic cause at the vesicoureteral junction [40]. There are three types of primary megaureter: obstructed primary megaureter, refluxing primary megaureter, and nonrefluxing unobstructed primary megaureter [2,40]. In primary obstructed megaureter, the most distal part of the ureter is adynamic and unable to conduct a peristaltic wave, producing a functional obstruction similar to that observed in achalasia or Hirschsprung's disease [40,41]. US features of primary megaureter include fusiform dilation of the distal third of the affected ureter proximal to its insertion into the bladder and a smooth, tapered, adynamic far distal ureter on real-time examination (Fig. 5) [3]. At cystoscopy, primary megaureter is characterized by a normal ureteral orifice without true organic narrowing of the distal ureter when probing with a ureteral catheter [40]. Ipsilateral megacalycosis and vesicoureteral reflux may also present. Primary megaureter of the nonobstructive variety can resolve spontaneously (Fig. 6) [42]. In such cases, primary megaureter is thought to be related to functional immaturity of the ureter [39].

Vesicoureteral reflux refers to the retrograde passage of urine from the urinary bladder to the ureter and often to the calyces [40]. Vesicoureteral reflux is thought to be caused by a developmental anomaly at the ureterovesical junction in which the ureteral orifice may be lateralized or too large or the submucosal ureter is too short or deficient in longitudinal muscle fibers [43]. Immaturity of the ureterovesical junction may contribute to some extent [43]. Patients with vesicoureteral reflux can present in the neonatal period with antenatally detected hydronephrosis or urinary tract infection. The severity of vesicoureteral reflux can be graded based on the appearance of the upper urinary tract on voiding cystourethrogram [44]. Vesicoureteral reflux can disappear spontaneously as the ureterovesical junction matures during the first decade of life. Mild vesicoureteral reflux (grade 1 and 2) has a favorable prognosis and disappears with time in more than 80% of cases, while more severe forms have a lower incidence of spontaneous resolution [43,45]. Vesicoureteral reflux associated with anatomic anomalies such as lateral ectopia of the lower moiety ureter in a duplex kidney or paraureteral diverticulum is not likely to resolve spontaneously. Vesicoureteral reflux is a risk factor for upper urinary tract infection and pyelonephritis with consequent renal scarring and potential long-term sequelae such as end-stage renal disease or hypertension.

The features of vesicoureteral reflux on conventional US are nonspecific. The walls of the renal pelvis and ureter may be thickened, presumably because of in-folding of the epithelium of the intermittently dilated collecting system during reflux while the dilated urinary tract empties [46]. The finding of a changing degree of hydronephrosis or hydroureteronephrosis may indicate the presence of vesicoureteral reflux. However, there is no one pathognomonic feature for the definitive diagnosis of vesicoureteral reflux on conventional US (Fig. 7) [4], and it is important to realize that a normal urinary sonogram dose not exclude reflux [40]. Therefore, contrast-enhanced voiding US, which assists with diagnosis and grading of vesicoureteral reflux while avoiding exposure to ionizing radiation, and can detect vesicoureteral reflux directly, may also be indicated [47,48]. This modality involves instillation of contrast material into the urinary bladder via catheter and monitoring of its retrograde passage from the bladder to the ureter and the renal pelvis via alternatively scanning both kidneys and the bladder during filling and before and after voiding.

Multicystic dysplastic kidney is a subtype of renal dysplasia characterized by the presence of multiple, variable sized, noncommunicating cysts in the absence of normal renal parenchyma (Fig. 8) [49]. Severe ureteral obstruction early in the gestation period is thought to lead to this condition [38]. Most cases are correctly identified in utero with US [4]; postnatal US findings consistent with multicystic dysplastic kidney will also suffice to confirm the diagnosis in most cases [36]. In addition to confirming the diagnosis, postnatal US in neonates with a multicystic dysplastic kidney is also performed to check for associated anomalies in the contralateral unaffected kidney. Vesicoureteral reflux or ureteropelvic or ureterovesical junction obstruction has been reported in the contralateral kidney in up to 50% of cases, and such abnormalities are of great clinical concern [36]. Unlike severe hydronephrosis, in which the centrally located renal pelvis is the most greatly distended and communicates with the surrounding dilated calyces, the distribution of the cysts in cases of multicystic dysplastic kidney is without a recognizable pattern [38]. Multicystic dysplastic kidney usually shrinks or disappears spontaneously over time.

Duplex kidney defines a single renal unit that is drained by two collecting systems. Forms of duplex kidney range from bifid renal pelvis to incomplete or complete ureteral duplication [50]. Clinically, complete duplication may present with hydronephrosis in the neonatal period [2]. Cases of complete duplication will almost always follow the Weigert-Meyer rule, i.e., the ureter from the upper moiety inserts distally and medially and frequently ends as an ureterocele or an ectopic ureter while the ureter from the lower moiety inserts more cranially and laterally and often has a perpendicular course, predisposing it to reflux [40,41]. The ectopic ureter can insert into various locations according to gender, including bladder neck, urethra, vestibule, vagina, or uterus in girls, and bladder neck, posterior urethra, or genital ducts such as the seminal vesicle, vas deferens, or ejaculatory duct in boys [40].

Uncomplicated cases of duplex kidney may be difficult to diagnose by US. The affected kidney is often longer and has a prominent parenchymal column that appears to separate the sinus fat, which provides indirect evidence of collecting system duplication [50]. High-resolution US may allow direct visualization of two renal pelvises with two separate proximal ureters [51]. More commonly, complete duplications will present with upper moiety hydronephrosis (Fig. 9). Dilation of the lower moiety may be seen due to reflux or less often, concomitant ureteropelvic junction obstruction [52]. In this situation, an important diagnostic clue for duplex kidney is the uneven pelvocalyceal dilation, which is unlike the pelvocalyceal dilation seen in other urinary abnormalities. US of the bladder may show a thin-walled intraluminal cystic structure indicative of ureterocele, and occasionally the parenchyma of the upper moiety appears hyperechoic with small cysts caused by accompanying dysplasia [3].

Posterior urethral valve is the most common cause of urethral obstruction in male patients [53]. Posterior urethral valve is presumed to be due to congenital membranous folds of Wolffian duct origin that cause variable degrees of obstruction at the junction of the penile and posterior urethra [2,40]. It is suggested when prenatal US shows bilateral hydroureteronephrosis associated with a thick-walled bladder and oligohydramnios [2], and the postnatal diagnosis is typically confirmed by voiding cystourethrography demonstrating a dilated posterior urethra with an abrupt transition to a small bulbous urethra at the level of the valve [53]. A coarse, trabeculated bladder and severe bilateral vesicoureteral reflux are also noted on voiding cystourethrography. Similarly, US findings include bilateral hydroureteronephrosis, an irregular thick-walled urinary bladder with or without associated bladder diverticula, and a dilated prostatic urethra (Fig. 10) [3]. In young infants, transperineal US can image posterior urethral dilation more clearly than conventional transabdominal scanning [54]. Posterior urethral valve should always be suspected when bilateral severe hydroureteronephrosis is noted while imaging male infants. The prognosis may be poor. Early renal failure can occur due to renal dysplasia, and progressive renal failure can follow even after treatment, possibly due to abnormal bladder function [55].