16 THE FETAL GENITOURINARY TRACT
Structurally and functionally, the urogenital system can be divided into two entirely different components—the urinary system and the genital system. Both of these develop from a common mesodermal ridge of tissue, the intermediate mesoderm, along the posterior wall of the abdominal cavity. Initially, the excretory ducts of both systems enter a common cavity, the cloaca.1
Human embryos develop three sets of excretory organs or kidney systems during intrauterine life.1,3 The embryonic kidneys, which are formed in a cranial to caudal sequence, in order of appearance are the pronephros, the mesonephros, and the metanephros. The pronephros, analogous to the kidneys in primitive fishes and the mesonephros, which are well developed and analogous to the kidneys of amphibians, both regress in utero. The third set of kidneys, the metanephroi, become the permanent kidneys (Fig. 16-1).2,3
(Modified from Park JM: Normal and anomalous development of the urogenital system. In Walsh PC: Campbell’s Urology, 8th ed. Philadelphia, WB Saunders, 2002, p 1737. Copyright © 2002 Saunders, An Imprint of Elsevier; and Larsen WJ: Human Embryology. New York, Churchill Livingstone, 1997.) (Illustration by James A. Cooper, MD, San Diego, CA.)
The pronephros is seen in the 3rd week of development and completely degenerates by the start of the 5th week. The second kidney, the mesonephros, also regresses by the 4th month; however, it serves as an excretory organ for the embryo while the definitive kidney begins its development. Certain elements of the mesonephros are retained in the mature urogenital system as part of the reproductive tract.3
The metanephros, or definitive kidney, forms in the sacral region as a pair of new structures called the metanephric diverticulum or ureteric bud. It emanates from the distal portion of the mesonephric duct and comes in contact with and penetrates the metanephric mesenchymal blastema (metanephric mesoderm) at approximately the 28th day.2,3
The ureteric bud and metanephric mesoderm exert reciprocal inductive effects toward each other, and the proper differentiation of these structures depends on these inductive signals. The metanephric mesoderm induces the ureteric bud to branch, and in turn, the ureteric bud induces the metanephric mesoderm to condense and undergo mesenchymal-epithelial conversion. The nephron, which consists of the glomerulus, proximal tubule, loop of Henle, and distal tubule, is thought to derive from the metanephric mesoderm, whereas the collecting system, consisting of collecting ducts, calyces, pelvis, and ureter, is formed from the ureteric bud (see Fig. 16-1).3
The division of the ureteric bud results in the eventual pelvicalyceal patterns and their corresponding renal lobules. The first few divisions of the ureteric bud give rise to the renal pelvis, major and minor calyces, and collecting tubules. Thereafter, the first generations of collecting ducts are formed. When the ureteric bud first invades the metanephric mesoderm, its expanded end forms an ampulla that will eventually give rise to the renal pelvis. By the 6th week, the ureteric bud has bifurcated at least four times, yielding 16 branches. These branches then coalesce to form two to four major calyces extending from the renal pelvis. By the 7th week, the next four generations of branches also fuse, forming the minor calyces. By the 32nd week, approximately 11 additional generations of bifurcation have resulted in approximately 1 to 3 million branches, which will become the collecting duct tubules. In humans, although renal maturation continues to take place postnatally, nephrogenesis is completed before birth.3
During the 4th to 7th weeks of development, the cloaca is divided by the urorectal septum into the urogenital sinus anteriorly and the anal canal posteriorly. The urogenital sinus is divided into three parts, of which the upper and largest part is the urinary bladder. Initially the bladder is continuous with the allantois, but when the lumen of the allantois is obliterated, a thick fibrous cord, the urachus, remains and connects the apex of the bladder with the umbilicus. The next part is a somewhat narrow canal, the pelvic part of the urogenital sinus, which in the male embryo, gives rise to the prostatic and membranous parts of the urethra and the entire urethra in female embryos. The caudal urogenital sinus forms the phallic urethra in the male embryo and the distal vaginal vestibule in the female embryo.1,2
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 (Fig. 16-2).
During the second and third trimester, the bladder will empty and refill continuously every 25 to 30 minutes. This cycle can be monitored during the sonographic examination. 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. At the end of the pregnancy, this cycle decreases, especially in female fetuses possibly due to hormonal influence on the fetal bladder neck. This may induce a pseudomegabladder (see later) (Figs. 16-3 and 16-4).4,5
FIGURE 16-3 Fetal bladder in the second trimester (male fetus). A. Transverse scan through the fetal pelvis demonstrating the bladder (thick arrow) and the fetal sex (thin arrow). B. Color Doppler of the umbilical arteries at both sides of the bladder (arrow).
With the use of transvaginal probes, fetal anatomic structures can be visualized earlier than with transabdominal ultrasound (US). Therefore, the fetal kidneys can be demonstrated at approximately 11 weeks transvaginally and at 12 weeks using transabdominal probes. During the first trimester, the kidneys appear as hyperechoic oval structures at both sides of the spine (their hyperechogenicity can be compared to that of the liver or spleen) (Fig. 16-5). 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. This should always be demonstrated in fetuses older than 18 weeks. Prominent pyramids should not be misinterpreted as calyceal dilatation (Fig. 16-6). The fetal kidneys’ growth can be evaluated throughout pregnancy by measuring renal length and comparing it to normal charts. (As a simple rule, renal growth is 1.1 mm/gestational week.) During the second and third trimesters, the kidneys are easily identified by imaging the dorsolumbar spine and scanning on either side in parasagittal and transverse axial sections. Urine distending the renal pelvis may help in their identification. Under normal conditions, the fetal ureters are not visible.4–6
FIGURE 16-5 Fetal kidney, first trimester. Parasagittal scan of a first trimester fetus. The kidney appears as a hyperechoic small oval mass (thick arrow). The adrenal above it is hypoechoic (thin arrow). H, fetal head.
In addition to the visualization of the bladder and normal kidneys, the assessment of the urinary tract (UT) should include an evaluation of the amniotic fluid volume. After 14 weeks, two thirds of the normal amniotic fluid is produced by fetal urination and one third from pulmonary fluid. A normal volume of amniotic fluid is mandatory for proper development of the fetal lung. A normal sized thorax can be confirmed by measuring thoracic diameters or thoracic circumference.7
The overall prevalence of renal tract anomalies is estimated at 5/1000 births. The percentage is likely higher when considering transient anomalies. Anomalies involving the UT are numerous and variable. They can be isolated or appear in association with another organ system’s anomalies. Therefore, the sonographic examination should be as meticulous as possible in order to visualize possible associated features. These additional findings will determine the prognosis.8–14
Bilateral renal agenesis is incompatible with extrauterine life. This condition, at times referred to as Potter’s syndrome, results in pulmonary hypoplasia and musculoskeletal abnormalities. The diagnosis is based initially on anhydramnios after 15 weeks and on the nonvisualization of normal renal structures (Fig. 16-7). The bladder is empty (very rarely, a small fluid-filled structure can be observed in the fetal pelvis. It might correspond to retrograde filling of the bladder). Whenever there is a question as to whether the kidneys are present, fetal magnetic resonance imaging (MRI) may help with the diagnosis. Enlarged, globular adrenals should not be misinterpreted as dysplastic kidneys.15–18
FIGURE 16-7 Bilateral renal agenesis, third trimester. A. Transverse scan of the fetal abdomen. Marked oligohydramnios. No renal structure is visible. Sp, spine; St, stomach. B. Sagittal scan of the fetal trunk of the same patient. No renal structure is visible. Ch, chest.
Unilateral agenesis occurs in 1/500 pregnancies. At the time of sonography, a normal kidney will not be identified in either lumbar area. When no other complication or malformation is present, the prognosis for postnatal life is excellent (Fig. 16-8). 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” (see Fig. 16-8B). In case of left renal agenesis, the left colonic flexure occupies the empty lumbar fossa and should not be confused with a cystic kidney or a dilated ureter. Whenever one or both lumbar fossas are empty, the kidneys should be searched for in an ectopic location (see later) (noteworthy, renal agenesis can theoretically result from the in utero regression of multicystic renal dysplasia).19–21
FIGURE 16-8 A. Transverse axial scan in a fetus with unilateral renal agenesis. The kidney is not seen in the renal fossa (large arrow). Normal contralateral kidney (small arrows). B. Sagittal scan in the same patient. The adrenal gland (arrows) on the same side as the absent kidney, is now elongated in what has been described as “the lying down adrenal sign.”
When no complication occurs, renal duplication is a benign condition and should be considered a normal variant (Fig. 16-9). If complicated, it should included in the differential diagnosis of UT dilatation (see later).
There are various ectopic locations possible for the kidney. The ectopic kidney is recognizable thanks to its characteristic CMD. An ectopic kidney is usually smaller and may be malrotated. Complications such as dilatation or dysplasia do occur. One or both kidneys can be ectopic. The pelvic location is the commonest location for ectopic kidneys to appear (Fig. 16-10). Other ectopic locations include horseshoe, crossed fused ectopia (both kidneys lie on the same side), and intrathoracic ectopia. In horseshoe kidneys, a bridge of renal tissue can be visualized in front of the spine (Fig. 16-11). Crossed ectopia should be differentiated from duplex kidneys. In crossed (fused) ectopia, there is an angulation between the two kidneys, whereas in duplication, the two renal moieties lie in the same continuous plane (Fig. 16-12).22,23
Small kidneys (below −2 standard deviations [SDs]) are usually seen when hypoplasia or dysplasia (or both) resulting from an embryologic maldevelopment, secondary to reflux (reflux nephropathy), obstruction, or to an ischemic phenomenon is present. Small kidneys may also result from so-called tubular dysgenesis associated with the maternal ingestion of angiotensin II antagonists. The prognosis of small kidneys depends on the remaining renal function. Cases with oligohydramnios have the poorest prognosis.24,25
Dysplastic renal parenchyma appears hyperechoic and is often associated with parenchymal cysts. Dysplastic and ischemic kidneys are part of the differential diagnosis of hyperechoic kidneys (see later). The differential diagnosis of enlarged kidneys (above +2 SDs) includes renal dilatation, cystic kidneys, syndromes with organomegaly (i.e., Beckwith-Wiedemann syndrome) and renal tumors (see later).
Dilatation of the renal pelvis is a common finding on obstetric US. Its frequency is evaluated at approximately 1% to 4% of all pregnancies. Yet, all dilatations do not have the same clinical relevance; furthermore, their antenatal and postnatal evolution is variable. This has led to abundant and somewhat controversial literature about the best work-up and follow-up after birth.13,26,27
Various criteria are used in order to objectively evaluate renal dilatation. In our experience, the best criterion is the measurement of the anteroposterior diameter of the renal pelvis on a transverse scan of the fetal abdomen (Fig. 16-13). Using this measurement, several threshold values have been applied in order to be able to predict the postnatal outcome, especially in cases with moderate dilatation (less than 15 mm). Many authors agree that the upper limit should be 4 mm during the second and 7 mm during the third trimester of the pregnancy (see Figs. 16-13 to 16-15). These limits are set in order to detect not only patients that will need corrective surgery (in case of obstructive dilatation) but also the majority of fetuses and neonates presenting with vesicoureteric reflux. These patients are at risk for developing complications and eventually worsening renal function.27–35
FIGURE 16-13 Bilateral mild dilatation. (A) Illustration demonstrating the method for measuring the degree of dilatation. A transverse axial plane of section of the fetal abdomen is obtained and an anteroposterior measurement of the renal pelvis is obtained. (B) Transverse sonographic scan through both kidneys (K) demonstrating a mildly distended renal pelvis and the method of measuring the renal pelvis (arrows). Ab, fetal abdomen; Sp, spine.
(A, Illustration by James A. Cooper, MD, San Diego, CA.)
FIGURE 16-14 Bilateral asymmetric dilatation (case of ureteropelvic obstruction), third trimester. A. Transverse scan through fetal abdomen. Marked left (20 mm between calipers) and moderate right (10 mm) dilatation. Sp, spine. B. Sagittal scan through the left kidney. Marked pyelocalyceal dilatation. The renal cortex is thinned (2 mm) and hyperechoic suggesting dysplasia. Ch, fetal chest.
FIGURE 16-15 Massive right renal dilatation. Case of ureteropelvic obstruction. A. Transverse scan through the fetal abdomen demonstrating marked dilatation of the renal pelvis (36 mm between calipers). Sp, fetal spine. B. Sagittal scan through the dilated kidney measuring 72 mm between the calipers.
Pyelectasis refers to a visible renal pelvis below the significant threshold. During the second trimester, there are reports of this feature as a minor sign of chromosomal anomaly.32 Other sonographic evidence of an abnormality of the UT includes the visibility of the fetal ureter during pregnancy (Figs. 16-16 and 16-17) and the demonstration of an enlarged bladder (more than 3 cm length during the second and 5 cm during the third trimester) (Fig. 16-18).34,36
FIGURE 16-16 Ureteral dilatation (case of ureteropelvic obstruction). Transverse scan of the fetal abdomen demonstrating the dilated tortuous ureter (12 mm between the calipers). Ab, abdomen; B, bladder; Sp, spine.
Abnormalities resulting in dilatation of the UT can be found at any time during pregnancy. The degree of dilatation may increase or decrease during each trimester. Therefore, in order to screen all potentially abnormal cases, some authors advocate performing one sonographic examination during each trimester.33 This is controversial, because most abnormalities, particularly mild UT dilatation, do not change significantly during pregnancy and, therefore, are unlikely to alter pregnancy and fetal management.
Once dilatation of the collecting system has been detected in utero, the subsequent evaluation should answer three major questions: the origin of the dilatation, the coexistence of associated anomalies, and finally, the prognosis of the malformation. The most common cause for UT dilatation is ureteropelvic obstruction (UPJ). Other causes include ureterovesical junction obstruction (UVJ), vesicoureteric reflux (VUR), complicated duplex kidneys, and bladder outlet obstruction (BOO) (Table 16-1).
UPJ, ureteropelvic obstruction; UVJ, ureterovesical junction obstruction; VUR, vesicoureteric reflux.
In cases of UPJ obstruction, the renal pelvis is dilated. As mentioned earlier, the threshold measurement on a transverse scan of the kidney is 7 mm for mild dilatation, between 7 and 15 mm for moderate dilatation, and more than 15 mm for marked dilatation. The more dilated the system, the more likely there is to be a decrease in renal function after birth. Furthermore, thinned, hyperechogenic renal cortices with cysts often correspond to obstructive dysplasia and impaired function (Fig. 16-19). Yet, unfortunately, there is often no direct correlation between the renal appearance and postnatal function (see Figs. 16-14 and 16-15).34–38
FIGURE 16-19 Urinary tract obstruction produces a varied response from the kidneys. A. The kidney may remain normal in distal obstruction, without reflux. B. Pelvocaliectasis may attenuate the parenchymal thickness. C. The kidney may suffer cystic dysplasia (parenchymal cysts), become fibrotic (increased echogenicity), and cease to function (lack of pelvocaliectasis). D. Alternatively, it may undergo cystic dysplasia with parenchymal cysts and increased echogenicity but continue to have pelvocaliectasis and a thinned parenchyma. If no cysts are visible but the parenchyma is of greatly increased echogenicity, either with (E) or without (F) pelvocaliectasis, dysplasia is probably, but not invariably present.
(Illustration by James A. Cooper, M., San Diego, CA.)
Noteworthy, obstruction may lead to leakage (rupture of a renal calyx or even bladder), and to urinary extravasation either as a perirenal urinoma or as ascites. The functional significance of the leakage is not straightforward. In some instances, it may protect the renal parenchyma, whereas in others renal growth is impaired (Fig. 16-20).24,39,40
The main differential diagnosis of UPJ obstruction is nonobstructive dilatation (which is a postnatal diagnosis), multicystic dysplastic kidney (MDK) (part of cystic renal diseases, see below) and UVJ obstruction. Rarer differential diagnoses of UPJ obstruction are megacalycosis due to medullary hypoplasia (the calyces are more dilated than the renal pelvis) and infundibular stenosis (no medullary hypoplasia, but still calyceal dilatation).
The diagnosis of UVJ obstruction is based on the demonstration of a dilated ureter. Peristaltic waves modify the caliber of the ureter (see Fig. 16-16).12–14,36 The dilatation may increase in utero, but it usually decreases after birth. In most instances, it is not possible to differentiate between dilatation secondary to UVJ obstruction from that secondary to high-grade vesicoureteric reflux (see Fig. 16-17). A hint for a differential diagnosis is the variability of the diameter of the renal pelvis during one single examination. This would favor VUR.
Renal duplication is usually easy to demonstrate once dilatation has developed. Various complications may occur at the level of renal duplications; for instance, obstruction at the upper or lower moiety or MDK at the upper or lower moiety. Both can be associated with distal insertion of the ureter ending either as an ureterocele or into an ectopic extravesical insertion. The ureterocele is seen as a septum within the bladder. It may prolapse into the urethra and result in acute in utero obstruction. The parenchyma related to obstruction may be thinned and dysplastic. The ectopic extravesical insertion may be difficult to diagnose in utero (Figs. 16-21 and 16-22).41–44
FIGURE 16-21 Renal duplication — Obstructed upper pole and ectopic ureterocele (third trimester). A. Illustration demonstrating duplication of the collecting system. Typically the upper pole moiety is obstructed and the lower pole moiety often demonstrates reflux. The ureter from the upper pole moiety inserts more medial and caudal into the bladder than the ureter from the lower pole. This is referred to as the Meyer-Wiegert rule. Dilatation of the submucosal portion of the ureter results in a ureterocele. B. Sagittal scan through the left kidney demonstrating the dilated upper pole (UP) and normal lower pole (LP). C. Sagittal scan through the bladder (B) displaying the ureterocele (arrow).
(A, Illustration by James A. Cooper, M.D., San Diego, CA.)
FIGURE 16-22 Complicated duplex system, third trimester. A. Sagittal scan of the left kidney. Both the upper (Up) and lower pole (Lp) are dilated. Sp, fetal spine. B. Transverse scan of the fetal abdomen demonstrating the dilated kidney (K), the dilated ureters (U; they should not be confused with dilated intestinal tract), and the urinary bladder (B).
Finally, the level of UT obstruction can be located below the bladder. The most frequent cause in male fetuses is posterior urethral valves (PUVs). The condition may or not induce dilatation of the upper UT. The dilatation can be unilateral or bilateral, and may be related to obstruction or to VUR.45,46 The degree of associated dysplasia is also variable. There seems to be a correlation between cortical echogenicity and the degree of obstructive dysplasia (Figs. 16-19 and 16-23).37
FIGURE 16-23 Posterior urethral valves and obstructive dysplasia. A. Coronal scan demonstrates a distended bladder (Bl), dilated ureters (U) and a dilated posterior urethra (PU). B. Bilateral hydronephrosis and hyperechogenic kidneys suggesting dysplasia. C. A sonogram slightly later of one of the kidneys confirms obstructive cystic dysplasia (arrows).
In cases of obstruction, the bladder “reacts” in different ways: it can enlarge, its wall can thicken, or the bladder may rupture and urinary ascites appears; other protective decompressive mechanisms may develop through VUR, urinomas, extravasation, or recanalization of the urachus (Fig. 16-24).39
FIGURE 16-24 Posterior urethral valves and urinoma, third trimester. Transverse scan of the fetal abdomen. The bladder (B) is small and its wall thickened. At the level of the left kidney, a large urinoma (U) has developed. The right kidney (RK) is just moderately dilated. Sp, spine.
Bladder enlargement due to obstruction secondary to PUV must be differentiated from other causes of BOO and from other causes of large bladder without obstruction (Table 16-2). Urethral atresia may result in megacystis detected during the first trimester and oligohydramnios (see Fig. 16-18); the condition often has a poor prognosis. A dilated penile urethra may be seen. Megacystis-megaureter association is related to massive VUR (Fig. 16-25). In such a case, the amniotic fluid volume is normal. Megacystis-microcolon-hypoperistalsis syndrome is a rare condition occurring in female fetuses with a poor postnatal prognosis (see later).46–49
FIGURE 16-25 Megacystis megaureter association, third trimester. Transverse scan (A and B) of the fetal abdomen showing variation in the dilatation of the renal pelvis at two different moments during the same examination. The bladder (B) is markedly enlarged. At birth there was bilateral grade V reflux. Sp, spine.
Whenever a renal anomaly (mainly dilatation) is detected, a complete survey of the fetal anatomy should be performed in order to detect associated malformations that would indicate the need for chromosomal analysis or the possibility of polymalformative syndromes; both worsen the prognosis.10,50,51
In cases of dilatation, the prognosis will depend upon the type and extent of anomalies. Features of poor prognosis include early diagnosis, bilateral marked dilatation, persistently obstructed bladder, oligohydramnios, and secondary lung hypoplasia. Bilateral renal dilatation and BOO have an increased risk of associated chromosomal anomalies, and therefore, in such cases, an evaluation of fetal chromosomes may be warranted. The finding of associated hyperechogenic and cystic renal parenchyma is frequently but only partially informative (positive predictive value [PPV] = 59%, negative predictive value [NPV] = 56%) about renal function. Conversely, normal cortical echogenicity does not exclude dysplasia.
The role of measuring urinary electrolytes in the fetal urine obtained through transabdominal puncture is controversial. There are discrepancies in the predictive values of urine biochemistry owing to small sample size, variations in cutoff values, gestational age, and sampling frequency. Fetuses with renal damage show decreased urinary concentrating especially of sodium and calcium without clear convincing confirmation. Measurements of B2-immunoglobulin on C cystatin in the fetal urines allow a better accuracy (Table 16-3). The outcome of vesicoamniotic shunting is also controversial. Although technically relatively easy, the long-term results have not been convincing.52–56
|Sodium*||< 100 mg/dl|
|Chloride*||< 90 mg/dl|
|Osmolality*||< 200 mg/dl|
|Calcium†||< 8 mg/dl|
|β2-Microglobulin‡||< 4.0 mg/L|
|Total Protein§||< 20 mg/dl|
|Cystatin C¶||< 1 mg/L|
It is of utmost importance that any information relevant for the proper postnatal management is correctly transmitted to the postnatal team that will be in charge of the newborn. A variety of findings may be seen in the neonate after birth that suggest an abnormality of the UT (Table 16-4). After birth, some conditions require an immediate confirmation and therapeutic maneuvers. For instance, obstructive PUVs or prolapsed ectopic ureterocele into the urethra leading to oligoanuria necessitate immediate treatment. In case of such suspicions, US and a voiding cystourethrogram (VCUG) should be performed immediately after birth in order to confirm the anomaly.57
In all other cases, the work-up should be planned without emergency. There is controversy regarding the respective role of US and VCUG in the postnatal work-up. Some authors advocate the systematic use of a VCUG in every case of antenatal detection of UT dilatation; for others, only patients with persistent dilatation should undergo a VCUG.58,59 Whatever the choice, all patients are put under prophylactic antibiotic therapy until a final diagnosis and a final therapeutic decision is made.
Practically, we have applied an algorithm based on US examinations (Fig. 16-26). An US including the kidneys, bladder, and ureters should be performed during the first week of life in order to verify the UT abnormality. The sonographic analysis should be as detailed as possible, and any significant anomaly should lead one to perform a VCUG. If the examination is negative, a repeat sonographic examination should be performed at the age of 1 month. Again, if any abnormality is found, a VCUG should be performed, but if no anomaly is demonstrated, no further evaluation is needed. At this stage, any prophylactic antibiotic therapy should be stopped.60
The role of VCUG is clearly to detect vesicoureteric reflux that will render long-term follow-up and persistent prophylaxis necessary. This attitude is intended to reduce unnecessary complications that are associated with high grades of VUR. It will also demonstrate anomalies of the urethra and potentially abnormal ureteral endings. Follow-up studies include US (every 6 months for a period of 2 years) in order to verify renal growth, VCUG every year to monitor the reflux, and MAG3 isotopic studies in order to verify renal function.61–63
If no reflux is present, complementary imaging is necessary in order to determine the origin of the dilatation. Renal function is assessed through isotopic studies; the morphology of complex or complicated UT malformations are best evaluated by MRI. The technique is particularly helpful for the assessment of the severely dilated UT and complicated duplex systems with dilatation of the upper and lower pole moieties. Also, the technique is able to provide information on the functional status of the kidney. It will help the surgeon in optimizing treatment.64 After this evaluation and if a conservative attitude is elected, a sonographic follow-up is advised in order to follow renal growth and dilatation. It has been shown that a large proportion of UT dilatation resolves spontaneously.63