Barrier-Forming Potential of Epithelial Cells from the Exstrophic Bladder.

Bladder exstrophy (BEX) is a rare developmental abnormality resulting in an open, exposed bladder plate. Although normal bladder urothelium is a mitotically quiescent barrier epithelium, histologic studies of BEX epithelia report squamous and proliferative changes that can persist beyond surgical closure. The current study examined whether patient-derived BEX epithelial cells in vitro were capable of generating a barrier-forming epithelium under permissive conditions. Epithelial cells isolated from 11 BEX samples, classified histologically as transitional (n = 6) or squamous (n = 5), were propagated in vitro. In conditions conducive to differentiated tight barrier formation by normal human urothelial cell cultures, 8 of 11 BEX lines developed transepithelial electrical resistances of more than 1000 Ω.cm2, with 3 squamous lines failing to generate tight barriers. An inverse relationship was found between expression of squamous KRT14 transcript and barrier development. Transcriptional drivers of urothelial differentiation PPARG, GATA3, and FOXA1 showed reduced expression in squamous BEX cultures. These findings implicate developmental interruption of urothelial transcriptional programming in the spectrum of transitional to squamous epithelial phenotypes found in BEX. Assessment of BEX epithelial phenotype may inform management and treatment strategies, for which distinction between reversible versus intractably squamous epithelium could identify patients at risk of medical complications or those who are most appropriate for reconstructive tissue engineering strategies.

Rare Variants in BNC2 Are Implicated in Autosomal-Dominant Congenital Lower Urinary-Tract Obstruction.

Congenital lower urinary-tract obstruction (LUTO) is caused by anatomical blockage of the bladder outflow tract or by functional impairment of urinary voiding. About three out of 10,000 pregnancies are affected. Although several monogenic causes of functional obstruction have been defined, it is unknown whether congenital LUTO caused by anatomical blockage has a monogenic cause. Exome sequencing in a family with four affected individuals with anatomical blockage of the urethra identified a rare nonsense variant (c.2557C>T [p.Arg853∗]) in BNC2, encoding basonuclin 2, tracking with LUTO over three generations. Re-sequencing BNC2 in 697 individuals with LUTO revealed three further independent missense variants in three unrelated families. In human and mouse embryogenesis, basonuclin 2 was detected in lower urinary-tract rudiments. In zebrafish embryos, bnc2 was expressed in the pronephric duct and cloaca, analogs of the mammalian lower urinary tract. Experimental knockdown of Bnc2 in zebrafish caused pronephric-outlet obstruction and cloacal dilatation, phenocopying human congenital LUTO. Collectively, these results support the conclusion that variants in BNC2 are strongly implicated in LUTO etiology as a result of anatomical blockage.

22q11.2 duplications in a UK cohort with bladder exstrophy-epispadias complex.

The bladder exstrophy-epispadias complex (BEEC) comprises of a spectrum of anterior midline defects, all affecting the lower urinary tract, the external genitalia, and the bony pelvis. In extreme cases, the gastrointestinal tract is also affected. The pathogenesis of BEEC is unclear but chromosomal aberrations have been reported. In particular, duplications of 22q11.2 have been identified in eight unrelated individuals with BEEC. The current study aimed to identify chromosomal copy number variants in BEEC. Analyses was performed using the Affymetrix Genome-wide SNP6.0 assay in 92 unrelated patients cared for by two UK pediatric urology centers. Three individuals had a 22q11.2 duplication, a significantly higher number than that found in a control group of 12,500 individuals with developmental delay who had undergone microarray testing (p < .0001). Sequencing of CRKL, implicated in renal tract malformations in DiGeorge syndrome critical region at 22q11, in 89 individuals with BEEC lacking 22q11 duplications revealed no pathogenic variants. To date, 22q11.2 duplication is the genetic variant most commonly associated with BEEC. This is consistent with the hypothesis that altered expression of a single, yet to be defined, gene therein is critical to the pathogenesis of this potentially devastating congenital disorder.

Antegrade venography identifies parallel venous duplications in the majority of adolescents with varicocele.

PURPOSE: We performed intraoperative antegrade venography to assess the prevalence of internal spermatic venous malformations in adolescents with varicocele. MATERIALS AND METHODS: During a 2-year period 58 adolescent males with visible or palpable varicocele underwent antegrade venography before varicocele surgery. Antegrade venography was performed through a scrotal incision. A vein within the pampiniform plexus was cannulated and up to 1.75 mg/kg iohexol 300 mg/ml was injected to outline the entire length of the internal spermatic vein. The radiographs were reviewed and classified according to Bähren and Murray criteria. RESULTS: Of the patients 43 (74.1%) demonstrated parallel duplications (Murray classification type P) of the internal spermatic vein. This rate is higher than the 2% reported based on retrograde venography. Of the patients with parallel duplications 21 (48.8%) showed duplications arising superior to the iliac crest (subtype A) and 22 (51.2%) had a combination of proximal duplications (subtypes B and C). Ten patients (17.2%) had a single internal spermatic vein, 2 (3.4%) had lumbar collaterals and 3 (5.2%) had renal collaterals. CONCLUSIONS: Parallel duplication of the internal spermatic vein is a common finding on antegrade venography. The various levels of duplication need to be identified before treatment of varicocele to maximize the success of the procedure.

Bladder Neck Surgery is not Routinely Needed to Achieve Urinary Continence in Patients with Primary Epispadias.

BACKGROUND: This study aims at investigating the continence outcome in primary epispadias patients treated at a tertiary center. The authors hypothesized that additional continence procedures following primary epispadias repair is not routinely needed. METHODS: Patients treated for primary epispadias at the authors' institution between 2007 and 2019 and toilet trained, were identified from a prospective maintained database. Males underwent chordee correction, urethroplasty and glanuloplasty. Females underwent genitoplasty with reduction urethroplasty. If continence was not achieved by 4-5 years of age, pelvic floor muscle (PFM) biofeedback therapy was performed. Other continent procedures were discussed with family/patient if still incontinent. PRIMARY OUTCOME: urinary continence. SECONDARY OUTCOMES: PFM biofeedback therapy, continence surgery, hydronephrosis. Type of epispadias, age at repair and follow-up presented as median was also reported. RESULTS: Thirty-three patients (29 males) were included. Twelve had penopubic epispadias, 13 glanular/penile, 4 duplicated urethra, 4 females. Median age at repair: 2 years (IQR 1-3), at follow-up: 8 years (IQR 6-10). Daytime continence: 100 % in penile/glanular; 33 % in penopubic and 75 % in duplicated urethra. Nighttime continence: respectively 92 %, 50 % and 100 %. 24 % of males were intermittently incontinent. All patients except one voided urethrally. One patient underwent bladder neck closure, ileocystoplasty and Mitrofanoff. One girl achieved daytime continence, 2 were intermittently incontinent, one continuously incontinent. All were enuretic. 38 % of boys and 100 % of girls had biofeedback therapy. None had hydronephrosis/renal impairment. CONCLUSIONS: Most children with primary epispadias can achieve social urinary continence spontaneously or with the support of PFM biofeedback therapy. Other continence procedures should be reserved for patients who do not attain satisfactory continence. LEVEL OF EVIDENCE: Treatment study - level IV.

Urethral Plate Grafting for Deficient Urethral Plate in Exstrophy: An Alternative Method to Augment Urethral Plate.

INTRODUCTION: Short urethral plate remains a challenge in exstrophy management. We report our experience with urethral plate grafting in cases of exstrophy with deficient urethral plate. METHODS: Among the exstrophy patients treated at the authors' institutions (2018-2022), those with a short urethral plate were prospectively included. A short urethral plate was defined as a distance between the verumontanum and the base of the glans of less than 10 mm. Urethral plate grafting was performed electively before the exstrophy closure. The urethral plate was divided just distal to verumontanum, and a thin inner preputial or para-exstrophy skin graft was harvested and deployed to cover the defect. Exstrophy closure was subsequently performed. The following parameters were recorded: age at grafting, type of graft and age at exstrophy closure. Reported outcomes include success of closure, complications, and follow up. RESULTS: Six male patients were included in the study: 3 classic bladder exstrophy (CBE) and 3 cloacal exstrophy (CE). Median age at grafting was 9 (3-18) months. Inner preputial grafts were utilized in the 3 CBE patients, and para-exstrophy skin grafts were used for the 3 CE patients. There was no graft loss, and longer and wide urethral plate was seen in all cases. Median time to bladder exstrophy closure was 3 (3-13) months after grafting. CONCLUSION: Pre-closure urethral plate grafting represents a safe and effective option for exstrophy patients with a short or inadequate urethral plate.

Delayed primary repair of bladder exstrophy: ultimate effect on growth.

PURPOSE: Late referrals or unsuitable bladder templates often require delayed primary repair of bladder exstrophy. We investigated longitudinal bladder growth rates and eventual outcomes following this approach. MATERIALS AND METHODS: After institutional review board approval, we reviewed the medical records of patients with classic bladder exstrophy who underwent neonatal or delayed (more than 30 days) primary closure at our institution between 1970 and 2006. Clinical characteristics and annual cystographic bladder capacity before the continence procedure were compared. Failed primary exstrophy repairs were excluded. RESULTS: A total of 33 patients with available bladder capacity measurements underwent delayed exstrophy closure due to small bladder template in 18 (88% male) and late referral in 15 (80% male) at respective median ages of 305 days (range 86 to 981) and 172 days (31 to 676). They were compared to 82 patients (71% male) undergoing neonatal closure at a median of 2 days of life (range 0 to 27). Pelvic osteotomy was performed in 32 of 33 delayed closures. Longitudinal analysis of the bladder capacities demonstrated that, compared to neonatally closed cases, bladder capacities were on average 36 ml smaller in those with delayed repair due to small templates (p = 0.01) and 29 ml smaller in those with late referrals (p = 0.13). However, the rate of bladder growth did not differ significantly among the 3 groups. CONCLUSIONS: Delayed primary repair of exstrophy does not compromise the rate of bladder growth. However, children born with smaller templates will have overall smaller capacities and are less likely to undergo bladder neck reconstruction.

Narrowing the chromosome 22q11.2 locus duplicated in bladder exstrophy-epispadias complex.

INTRODUCTION: Bladder exstrophy-epispadias complex (BEEC) comprises a spectrum of anterior midline congenital malformations, involving the lower urinary tract. BEEC is usually sporadic, but families with more than one affected member have been reported, and a twin concordance study supported a genetic contribution to pathogenesis. Moreover, diverse chromosomal aberrations have been reported in a small subset of individuals with BEEC. The commonest are 22q11.2 microduplications, identified in approximately 3% of BEEC index cases. OBJECTIVES: We aimed to refine the chromosome 22q11.2 locus, and to determine whether the encompassed genes are expressed in normal developing and mature human urinary bladders. RESULTS: Using DNA from an individual with CBE, the 22q11.2 duplicated locus was refined by identification of a maternally inherited 314 kb duplication (chr22:21,147,293-21,461,017), as depicted in this image. Moreover, the eight protein coding genes within the locus were found to be expressed during normal developing and mature bladders. To determine whether duplications in any of these individual genes were associated with CBE, we undertook copy number analyses in 115 individuals with CBE without duplications of the whole locus. No duplications of individual genes were found. DISCUSSION: The current study has refined the 22q11.2 locus associated with BEEC and has shown that the eight protein coding genes are expressed in human bladders both during antenatal development and postnatally. Nevertheless, the precise biological explanation as to why duplication of the phenocritical region of 22q11 confers increased susceptibility to BEEC remains to be determined. The fact that individuals with CBE without duplications of the whole locus also lacked duplication of any of the individual genes suggests that in individuals with BEEC and duplication of the 22q11.2 locus altered dosage of more than one gene may be important in BEEC etiology. CONCLUSIONS: The study has refined the 22q11.2 locus associated with BEEC and has shown that the eight protein coding genes within this locus are expressed in human bladders.

A genome-wide association study with tissue transcriptomics identifies genetic drivers for classic bladder exstrophy.

Classic bladder exstrophy represents the most severe end of all human congenital anomalies of the kidney and urinary tract and is associated with bladder cancer susceptibility. Previous genetic studies identified one locus to be involved in classic bladder exstrophy, but were limited to a restrict number of cohort. Here we show the largest classic bladder exstrophy genome-wide association analysis to date where we identify eight genome-wide significant loci, seven of which are novel. In these regions reside ten coding and four non-coding genes. Among the coding genes is EFNA1, strongly expressed in mouse embryonic genital tubercle, urethra, and primitive bladder. Re-sequence of EFNA1 in the investigated classic bladder exstrophy cohort of our study displays an enrichment of rare protein altering variants. We show that all coding genes are expressed and/or significantly regulated in both mouse and human embryonic developmental bladder stages. Furthermore, nine of the coding genes residing in the regions of genome-wide significance are differentially expressed in bladder cancers. Our data suggest genetic drivers for classic bladder exstrophy, as well as a possible role for these drivers to relevant bladder cancer susceptibility.

Effect of failed initial closure on bladder growth in children with bladder exstrophy.

PURPOSE: Failed initial bladder exstrophy closure may hinder the natural course of bladder growth compared to successful primary reconstruction. By measuring successive bladder capacities within the first 5 years of life, we compared the rate of bladder growth in children with failed vs successful initial closure. MATERIALS AND METHODS: We used an approved bladder exstrophy database to identify and review retrospectively patients with classic bladder exstrophy who underwent repeat cystograms between ages 1 and 6 years. Two groups of patients were identified--those with successful neonatal closure (group 1) and those with successful reclosure after an initial failed procedure (group 2). A generalized linear mixed model was fit to evaluate the impact of treatment group and age on bladder growth. RESULTS: We identified 48 patients in group 1 (75% male) and 62 in group 2 (71% male). Initial pelvic osteotomy was done in 60% of group 1 and 34% of group 2. Patients in group 1 had significantly larger cystographic capacity at 2, 4, 5 and 6 years after successful bladder closure compared to those in group 2 (p <0.05). The bladder tended to grow at a significantly slower rate in group 2 (9.38 cc yearly) compared to group 1 (14.76 cc yearly, p = 0.005). CONCLUSIONS: Patients with initial failed bladder exstrophy closure showed significantly smaller cystographic capacities and slower bladder growth compared to those who underwent successful neonatal bladder closure. These data clearly underscore the importance of a secure, successful primary closure.

Altered cytoskeletal structure of smooth muscle cells in ureteropelvic junction obstruction.

PURPOSE: Ureteropelvic junction obstruction is one of the most common causes of hydronephrosis in children. A malfunction of smooth muscle cells is believed to be the underlying mechanism causing obstruction. We investigated the expression of some integrins, talin and ß-dystroglycan, considered the main compound of smooth muscle cell cytoskeleton, and active caspase 3 at the level of the ureteropelvic junction obstruction. MATERIALS AND METHODS: Specimens were obtained at pyeloplasty in 12 children with ureteropelvic junction obstruction. Six control specimens were obtained during organ explantation. Specimens were divided into renal pelvis, ureteropelvic junction and ureter below the obstruction. Western blot analysis of active caspase 3, and immunofluorescence and polymerase chain reaction analysis were performed for α7A, ß1A, α7B and ß1D integrins, talin and ß-dystroglycan. RESULTS: Talin and ß-dystroglycan were slightly impaired in ureteropelvic junction obstruction, while α7B and ß1D integrins were severely reduced, and α7A, ß1A and active caspase 3 were significantly enhanced compared to controls. CONCLUSIONS: We demonstrated activation of apoptosis and a critical alteration of cytoskeleton that might explain the altered function and the increased apoptosis in smooth muscle cells in ureteropelvic junction obstruction. The delayed rearrangement of the cytoskeleton of smooth muscle cells in ureteropelvic junction obstruction might be linked to a postnatal splicing from α7A and ß1A to α7B and ß1D integrins, respectively. This relationship could explain the common clinical scenario of spontaneous improvement of hydronephrosis in children with suspected ureteropelvic junction obstruction.

The Genomic Architecture of Bladder Exstrophy Epispadias Complex.

The bladder exstrophy-epispadias complex (BEEC) is an abdominal midline malformation comprising a spectrum of congenital genitourinary abnormalities of the abdominal wall, pelvis, urinary tract, genitalia, anus, and spine. The vast majority of BEEC cases are classified as non-syndromic and the etiology of this malformation is still unknown. This review presents the current knowledge on this multifactorial disorder, including phenotypic and anatomical characterization, epidemiology, proposed developmental mechanisms, existing animal models, and implicated genetic and environmental components.

Novel approach to vaginal calculus in a girl with urogenital sinus anomaly.

Isolated urogenital sinus can cause distended bladder and/or vagina and may present with an abdominal mass and sepsis during infancy. Older children may present with recurrent urinary tract infections and hematocolpos. We describe a 3-year-old girl with recurrent urinary tract infections thought to be secondary to vesicoureteric reflux. On further investigation, an isolated urogenital sinus anomaly with a calculus inside one of the hemivaginae was noted. She was managed expectantly with a plan to intervene at puberty. At puberty, during removal of the stone, the hemivaginal introitus was found to be stenotic. Gradually increasing sizes of Amplatz type graduated renal dilators were introduced from the introitus of the urogenital sinus into the hemivaginal stone until a size 22F Amplatz sheath could be passed easily. Size 10F cystoscope was passed through this channel, and the stone was fragmented using electrohydraulic lithotripsy. At a later date, she underwent staged anterior sagittal transvulval mobilization of the urogenital sinus.

SLC20A1 Is Involved in Urinary Tract and Urorectal Development.

Previous studies in developing Xenopus and zebrafish reported that the phosphate transporter slc20a1a is expressed in pronephric kidneys. The recent identification of SLC20A1 as a monoallelic candidate gene for cloacal exstrophy further suggests its involvement in the urinary tract and urorectal development. However, little is known of the functional role of SLC20A1 in urinary tract development. Here, we investigated this using morpholino oligonucleotide knockdown of the zebrafish ortholog slc20a1a. This caused kidney cysts and malformations of the cloaca. Moreover, in morphants we demonstrated dysfunctional voiding and hindgut opening defects mimicking imperforate anus in human cloacal exstrophy. Furthermore, we performed immunohistochemistry of an unaffected 6-week-old human embryo and detected SLC20A1 in the urinary tract and the abdominal midline, structures implicated in the pathogenesis of cloacal exstrophy. Additionally, we resequenced SLC20A1 in 690 individuals with bladder exstrophy-epispadias complex (BEEC) including 84 individuals with cloacal exstrophy. We identified two additional monoallelic de novo variants. One was identified in a case-parent trio with classic bladder exstrophy, and one additional novel de novo variant was detected in an affected mother who transmitted this variant to her affected son. To study the potential cellular impact of SLC20A1 variants, we expressed them in HEK293 cells. Here, phosphate transport was not compromised, suggesting that it is not a disease mechanism. However, there was a tendency for lower levels of cleaved caspase-3, perhaps implicating apoptosis pathways in the disease. Our results suggest SLC20A1 is involved in urinary tract and urorectal development and implicate SLC20A1 as a disease-gene for BEEC.

Outcome study of lower pole heminephrectomy in children.

OBJECTIVE: This study assessed the role and long-term outcome of lower pole heminephrectomy in the treatments of non-functioning lower renal moieties in children with duplex kidneys. MATERIAL AND METHODS: In a period of 10 years 31 lower pole heminephrectomies were performed in 30 patients with duplex systems. Eight patients were diagnosed prenatally, 24 patients (80%) presented with urinary tract infection and three (10%) with vomiting and failure to thrive, and five patients also had other symptoms. The indication for lower pole heminephroureterectomy was reflux nephropathy in non-functioning lower pole in 28 patients (93%), pelviureteric junction obstruction in one patient (3%) and cystic dysplasia in one patient (3%). The surgical technique used was a combination of anterolateral loin incision plus right or left inguinal incision in 28 patients (90%). RESULTS: The operative course was uneventful, no blood transfusion were required, and no damage to the upper pole moiety or upper pole ureter was observed. Four patients (13%) had immediate postoperative complications and three (10%) had late postoperative complications. Long-term follow-up revealed no complications in 27 patients (90%) and three patients (10%) with increased urinary frequency. CONCLUSIONS: The results indicate that lower pole heminephrectomy is the treatment of choice in cases of non-functioning dilated lower segments of duplicated kidneys. The use of two incisions in this procedure is effective in preventing the need for further surgical treatment secondary to complications of the stump.

Distribution of Semen Parameters Among Adolescent Males Undergoing Fertility Preservation in a Multicenter International Cohort.

OBJECTIVE: To determine the distribution of semen parameters among adolescent and adult males presenting for fertility preservation. METHODS: A retrospective, cross-sectional cohort study of adolescent males age 11-19 who underwent semen analysis for fertility preservation at 3 centers in 2 countries with a comparison cohort of adult men presenting for fertility preservation. Prevalence of azoospermia and distribution of semen parameters was compared across groups. RESULTS: A total of 197 adolescents and 95 adults underwent semen analysis for fertility preservation. Azoospermia was present in 17 (8.6%) adolescents and 3 (3.2%) adults. There was decline in the prevalence of azoospermia with increasing age. After exclusion of patients with azoospermia, the adolescent and adult cohorts were comprised of 180 and 92 patients, respectively. Median age at presentation among adolescents vs adults was 16.5years (interquartile range [IQR] 15.2-17.6) and 30.8years (IQR 22.7-43.8), respectively. Median semen volume was 1.0mL (IQR 0.5-2.0) vs 2.5mL (IQR 1.5-3.5), P <.001. Median sperm concentration was 30million/mL (IQR 10-57) vs 39million/mL (IQR 14-57), P = .2. Median sperm motility was 39% (IQR 20-55) vs 45% (IQR 35-55), P = .01. Median total motile sperm count was 11million (IQR 1.4-33) for adolescents vs 29million (IQR 13-69) for adults, P <.001. CONCLUSION: Young adolescent males had higher prevalence of azoospermia and lower semen parameters compared to adults. In conjunction with physical examination, Tanner stage, and specific clinical context, these data can help to inform patients and their families about potential for fertility preservation, even in very young adolescent patients.

Salvage procedures to achieve continence after failed bladder exstrophy repair.

PURPOSE: We assessed the results from a single exstrophy center of salvage continence surgery after failed staged reconstruction for bladder exstrophy. MATERIALS AND METHODS: A total of 32 patients with bladder exstrophy had undergone salvage continence procedures. Indications for surgery included incontinence due to poor bladder capacity or failed bladder neck repair, and upper tract deterioration. Continence was defined according to the International Children's Continence Society as continent, intermittently incontinent and continuously incontinent. RESULTS: A total of 29 patients (91%) are continent, 3 (9%) are intermittently incontinent and none is continuously incontinent. One patient is continent after bladder augmentation and urethral clean intermittent catheterization. Two patients are continent and 1 is intermittently incontinent after bladder augmentation and modified Young-Dees bladder neck repair using urethral clean intermittent catheterization. One patient is continent using clean intermittent catheterization through a continent cutaneous diversion into a bladder substitution. A total of 19 patients are continent after bladder neck closure, bladder augmentation and continent cutaneous diversion using clean intermittent catheterization. Four patients are continent after cutaneous urinary diversion. Two are continent and 2 are intermittently incontinent after a Mainz II pouch. CONCLUSIONS: The majority of patients can still achieve continence following failed staged repair. Patients who have a low bladder leak pressure and who tolerate urethral catheterization can be consistently dry with bladder augmentation and bladder neck repair, which is a viable alternative to bladder neck closure, bladder augmentation and continent cutaneous diversion. Cutaneous urinary diversion has a role in selected patients. Mainz II pouch has not yielded consistent results. With better patient selection and increasing experience within specialist exstrophy centers fewer patients should require salvage continent surgery in the future.

An unusual bladder/cloacal exstrophy with urachal exstrophy.

The authors report a previously unpublished association of bladder exstrophy with cleft lip, exomphalos, Meckel's diverticulum imperforate anus, and a large urachal mass protruding below the umbilicus. The baby underwent surgical repair of the condition and the postoperative recovery was uneventful. None of the theories formulated to explain the embryogenesis of bladder exstrophy can explain these findings. The abnormality is within the bladder exstrophy/cloacal exstrophy spectrum.

Financial analysis of laparoscopic versus open nephrectomy in the pediatric age group.

The authors compared the cost of laparoscopic nephrectomy to open nephrectomy in the pediatric age group. One hundred seventeen consecutive laparoscopic nephrectomies performed by a surgeon with extensive experience with this approach between April 2003 and August 2006 were included. A control group of 24 consecutive open nephrectomies performed by urologists who do not use the laparoscopic approach were also included. Inclusion criteria for surgery were a poor or nonfunctioning kidney related to severe obstructive or refluxing nephropathy and a multicystic dysplastic kidney. The length of operation, length of stay, and disposable equipment used were recorded and the different approaches were compared statistically with an unpaired t test. The mean (standard deviation [SD]) duration of the procedure was 79 minutes (32) in the laparoscopic group and 85 minutes (35) in the control group (P = 0.41). The mean (SD) cost of the disposable instruments used during the operation was pounds sterling274 (160) in the laparoscopic group and pounds sterling20 (5) in the control group (P = 0.0001). The mean (SD) hospital stay was 1 night (0.43) with a mean (SD) cost of pounds sterling677 (291) in the laparoscopic group, and 3 nights (2) with a mean (SD) cost of pounds sterling2031 (1354) in the control group (P = 0.0001). The mean (SD) total cost of the procedure was pounds sterling951 (451) for the laparoscopic group and pounds sterling2051 (1359) for the open one (P = 0.0001). In our experience, the laparoscopic approach in the pediatric age group is 54% less expensive than the open approach.

Constant urinary dribbling due to an ectopic ureter and delays in diagnosis.

We present 2 patients who had a solitary kidney visualized on ultrasound imaging and experienced constant urinary dribbling. Further imaging modalities defined the anatomy and visualized the contralateral kidney and ectopic ureter causing the dribbling. Both patients went on to have curative surgical procedures. These cases reinforce the point that in a toilet-trained girl with normal voiding at normal intervals experiencing constant urinary dribbling, the diagnosis of an ectopic ureter must be considered early and referral made for appropriate imaging. Because of the abnormal anatomy, ultrasound imaging is particularly limited in such cases, but if used, one should take account of antenatal and postnatal scans. Referral is advocated, based on history alone, for appropriate imaging and investigation.