Year : 2009 | Volume
: 20 | Issue : 2 | Page : 246--250
Causes and outcome of prenatally diagnosed hydronephrosis
Ali Ahmadzadeh1, Morteza Tahmasebi2, Mohammad Momen Gharibvand2,
1 Pediatric Nephrology Unit, Abuzar Children’s Hospital, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
2 Radiology Department, Golestan Medical Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Pediatric Nephrology Unit, Abuzar Children’s Hospital, Jundishapur University of Medical Sciences, Ahvaz
Hydronephrosis is the most common abnormal finding in the urinary tract on prenatal screening with ultrasonography (U/S). Hydronephrosis may be obstructive or nonobstructive; obstructive lesions are more harmful to the developing kidneys. The aim of the study was to evaluate the causes of renal pelvic dilatation and the outcome of postnatal treatment in infants with hydronephrosis diagnosed prenatally with U/S. We prospectively studied 67 (60 males) newborns with hydronephrosis diagnosed prenatally and confirmed postnatally with U/S from Sept. 2005 to Oct. 2007. The patients were allocated to three groups based on the measurement of the anteroposterior renal pelvic diameter (APRPD) in transverse plane: mild (6-9.9 mm), moderate (10-14.9 mm) and severe (> 15 mm) hydronephrosis. Voiding cystourethrography (VCUG) was obtained in all of the patients to rule out vesicoureteral reflux (VUR). In cases with negative VUR, Diethylenetriamine-pentaacetic acid (DTPA) scan with diuretic renography was performed to detect ureteropelvic joint obstruction (UPJO). Twenty two cases (32.8%) had mild, 20 (29.9%) had moderate, and 25 (37.3%) had severe hydronephrosis. The causes of hydronephrosis were VUR (40.2%), UPJO (32.8%), posterior urethral valves (PUVs) (13.4 %), and transient hydronephrosis (13.4 %). The lesion was obstructive in 37 (55.2%) infants. Totally, 33 (49.2%) patients with hydronephrosis (9 mild, 9 moderate, and 15 severe) subsequently developed complications such as UTI and renal insufficiency, or required surgery. Associated abnormalities were observed in 15 (22.4%) patients. We conclude that every newborn with any degree of hydronephrosis should be assessed postnatally for specific diagnosis and treatment.
|How to cite this article:|
Ahmadzadeh A, Tahmasebi M, Gharibvand MM. Causes and outcome of prenatally diagnosed hydronephrosis.Saudi J Kidney Dis Transpl 2009;20:246-250
|How to cite this URL:|
Ahmadzadeh A, Tahmasebi M, Gharibvand MM. Causes and outcome of prenatally diagnosed hydronephrosis. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2020 Jul 5 ];20:246-250
Available from: http://www.sjkdt.org/text.asp?2009/20/2/246/45572
The introduction of fetal ultrasonography (US) has allowed for the detection of many intrauterine anomalies. Indeed, most anomalies are detected during routine fetal US done from 18-20 weeks of gestation.
Urinary tract anomalies are readily identified, and hydronephrosis is the most common anomaly comprising 50% of congenital malformations.  Intuitively, hydronephrosis is found in 0.59%  to 1.4% of fetuses,  and is considered obstructive in nature. However, antenatal hydronephrosis can be the result of nonobstructive processes such as vesicoureteral reflux (VUR), non-refluxing non-obstructed megaureter, and prune belly syndrome.
Bilateral obstructive lesions are more harmful to the developing kidneys than unilateral ones since urine is a major component of amniotic fluid and necessary for normal lung development and prevention of compression deformities. However, many cases of congenital hydronephrosis improve or resolve spontaneously without surgical intervention.  Therefore, differentiation of obstructive lesions and non-obstructive lesions is extremely important in determining the outcome of the fetuses. ,
We aim in this study to evaluate causes of renal pelvic dilatation (RPD), renal function, and need for postnatal (medical and or surgical) treatment in infants with hydronephrosis diagnosed with US.
Methods and Subjects
We prospectively studied 70 newborns with congenital hydronephrosis from Sept. 2005 to Oct. 2007.
Inclusion criteria included unilateral or bilateral anterio-posterior renal pelvis diameter (APRPD) diagnosed prenatally (6 mm in the third trimester) and confirmed postnatally with US, which was performed in all of the patients at least one time on the day between 5-10 of postnatal life.
Exclusion criteria included perinatal death, incomplete data and no written informed consent obtained from the parents. All of the ultrasound examinations were done by the two expert ultrasonographists in the radiology departments of Imam Khominee and Golestan hospitals.
We used Hitachi 525 ultrasound machine, prenatally with probe 3.5 MHZ and postnatally with 5-10 MHZ. Postnatally, the patients were allocated to three groups based on APRPD measured in transverse plane: mild (6-9.9 mm), moderate (10-14.9 mm), and severe (> 15 mm) hydronephrosis.
Voiding cystourethrography (VCUG) was performed in all of the patients to rule out VUR. In cases with negative VUR, Diethylenetriamine-pentaacetic acid (DTPA) scan with diuretic renography was performed to detect ureteropelvic joint obstruction (UPJO).
Renal function was assessed with both serum creatinine level corrected to age and DTPA scan. Prior to diuretic renography, serum creatinine was measured to confirm the absence of renal dysfunction. Patients should be at least 1 month of age during this assessment because newborns have a low glomerular filtration rate (GRF), and the dilatation can be mistaken for occlusive type due to immature excretory function. Also, newborns could respond poorly to diuretics. 
Statistical analysis of data was performed by using the SPSS (version 14) program. P values 15/25 (60%) with severe hydronephrosis had UTI, renal insufficiency or required surgery. Associated abnormalities were observed in 15 (22.4%) patients; 4/22, 8/20, and 3/25 in the three groups, respectively. Finally, 12 (18%) infants had no underlying abnormality, 9 with a transient hydronephrosis and 3 with a non-obstructive hydronephrosis.
In the appearance of intrauterine hydronephrosis was first described by Garrett et al. in 1975.  Since then, others authors have documented the ability of US to detect this condition in utero. , In our series, out of 67 newborns, 55 (82%) had an underlying pathology, which was close in incidence to the study conducted by Aksu et al who reported an underlying pathology in 75.1% of newborns with congenital hydronephrosis. 
In our study, 60% of the infants were males. Essentially, obstructive lesions were more common in males and PUVs were only seen in boys. In our series, 9 (13.4%) had PUVs, but the other lesions were also more common in the gender.
In the present study, the most common causes of dilation of renal pelvis were VUR (40.2%) and UPJO (%32.8), which were not consistent with the study of Aksu who found UPJO in 62.7% and VUR in 16.6% of cases. However, Woodward and Frank  recently reported 11% UPJO and 9% VUR.
Multicystic dysplastic kidney is a separate anomaly potentially confused with the hydronephrosis prenatally. Our findings were not comparable with the study of Woodward particularly in the rate of transient hydronephrosis (13.4% vs 48%). However, in our study, 37 (55.2%) infants had obstructive lesions 22 UPJO, 5 UVJO, 9 PUVs, and one idiopathic megaureter representing the role of US in detection and early relief of the obstructive process.
Obstructive uropathy occurs in 1 in 1000 live births and accounts for 23% of chronic renal insufficiency in children. Nearly 7% of neonatal deaths occur in infants with major renal and urinary tract anomalies. , Obstruction induces the renin-angiotensin-aldosterone system, causing vasoconstriction, interstitial fibrosis, and ischemic atrophy as well as induction of apoptosis in the obstructed kidney.
While early correction of the obstructive process is followed by a significant hemodynamic recovery. , In the present study, hydronephrosis was confirmed postnatally in all the 67 fetuses with suspected hydronephrosis i.e. there was a good correlation between the prenatal and postnatal US findings. The diagnosis was mainly on the basis of measurement of the APRPD with US. Our findings showed that APRPD was a simple and sensitive technique for prerenal diagnosis of congenital hydronephrosis, allowing identification of 100% of cases. Therefore, postnatal follow-up studies are warranted if an APRPD is greater than or equal 6 mm in the third trimester.
The rate of mildly dilated kidneys diagnosed prenatally decreased from 60% to 27.2% postnatally. While, the rate increased in both the moderate and severely dilated groups from 21.1% and 18.9% to 36.4% in each. This indicates that mildly dilated kidneys should also be carefully followed up as the more severe groups.
We conclude that our study demonstrates the most common causes of hydronephrosis in fetuses. These include VUR, UPJO, PUVs and transient hydronephrosis. Postnatal assessment of infants with hydronephrosis facilitates the correct determination of the nature and site of the lesion, and allows an appropriate management. We believe that every newborn with any degree of hydronephrosis should be assessed postnatally.
The authors would like to thank Dr. Dawoodi for assisting in U/S examinations at Imam, s Khomimee hospital and Mr. Cheraghian for statistical analysis of the results.
MGM participated in data collection. TM helped in US examinations, analysis and interpretation of the data. AA participated in data collection analysis, interpretation of the data and also draft of the manuscript.
This study was supported by the vice- chancellor for research affairs, Ahvaz Jundishapur University of Medical Sciences.
|1||Liang CC, Cheng PJ, Lin CJ, Chen HW, Chao AS, Chang SD. Outcome of prenatally diagnosed fetal hydronephrosis. J Reprod Med 2002;(47):27-32.|
|2||Woodward M, Frank D. Postnatal management of antenatal hydronephrosis. BJU Int 2002; (89):149-56.|
|3||DiSandro MJ, Kogan BA. Neonatal management: Role for early intervention. Urol Clin North Am 1998;25(2):187-97.|
|4||Diamond DA, Peters CA. Perinatal urology, In: Avener ED, Harmon WE, Niaudet P (eds). Pediatric Nephrology, 5th edn, Philadelphia, Lippincott William &Wilkins 2004:73-80.|
|5||Chevalier R. Obstructive uropathy. In: Kher KK, Schnaper HW, Makker SP (eds). Clinical Pediatric Nephrology 2nd edn, Informa healthcare, 2006:507-16.|
|6||Shimada K, Kakizaki H, Kubota M, et al. Standard method for diagnosing dilatation of the renal pelvis and ureter discovered in the fetus, neonate or infant. Int J Urol 2004;11 (3):129-36.|
|7||Garrett WJ, Kossoff G, Osborn Ra. The diagnosis of fetal hydronephrosis, megaureter and urethral obstruction by ultrasounic echography. Br J Obstet Gynecol 1975;82:115-20.|
|8||Sanders R, Graham D. Twelve cases of hydronephrosis in utero diagnosed by ultrosonography. J Ultrasound 1982;1:341-8.|
|9||Blane Ce, Koff SA, Bowerman RA, Barr M. Nonobstructive fetal hydronephrosis: Sonographic recognition and therapeutic implications. Radiology 1983;147:95-9.|
|10||Aksu N, Yavascan O, Kanqin M, et al. Postnatal management of infants with antenatally detected hydronephrosis. J Pediatr Nephrol 2005; 20:1253-2.|
|11||Woodward M, Frank D. Postnatal management of antenatal hydronephrosis. BJU Int 2002;89 (2):149-56.|
|12||Chevalier RL, Chung KH, Smith CD, et al. Renal apoptosis and clusterin following ureteral obstruction: The role of maturation. J Urol 1996;156(4):1474-9.|
|13||Chevalier RL, Gomez RA, Jones CE. Developmental determinants of recovery after relief of partial ureteral obstruction. Kidney Int 1988;33(4):775-81.|