Postnatal Follow-Up of Hydronephrosis Detected by Prenatal Ultrasound: The Natural History

Kitagawa, Hiroaki; Pringle, Kevin C.; Stone, Peter; Flower, Jennifer E.; Murakami, Nobuya; Robinson, Richard D.

doi:10.1159/000020795

Cited by 54 publications

(30 citation statements)

References 26 publications

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“…16 Three small prospective studies recognized that 10 to 30% of their ANH infants were lost to follow-up. 2,12,[17][18] More recently Lee et al, 3 in a meta-analysis (using a criteria similar to ours) noted that 246 (15%) of 1678 patients with ANH were lost to follow-up. Many investigators, however, have not mentioned any loss of patients in their ANH programs.…”

Section: Discussionsupporting

confidence: 52%

Postnatal follow-up of antenatal hydronephrosis: a health-care challenge

et al. 2009

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Objective: To examine our experience with ANH and to determine the success of our postnatal follow-up program.Study Design: Charts of mothers and infants seen (2004 to 2008) at our Regional Perinatal Center were reviewed retrospectively. ANH was defined during the third trimester by anterior pelvic diameters as follows: mild 7 to 9, moderate 10 to 14 or severe X15 mm. Fetuses with multicystic dysplastic kidney (MCDK) were included. Result:Screening of approximately 15 000 ultrasound (US) reports identified 268 fetuses with ANH. After prenatal US surveillance, 88 (33%) fetuses had resolved, while 180 (67%) required postnatal follow-up. These 180 fetuses were diagnosed with mild 38 (21%), moderate 83 (46%) and severe 19 (11%) ANH, uni or bilateral hydroureters 12 (7%), MCDK 19 (10%) and miscellaneous 9 (5%). Postnatal follow-up was successfully established for 75% of infants with hydroureters, 68% for those with MCDK and for 37% of infants with mild, 53% with moderate and 58% with severe ANH. Factors commonly known to influence compliance were not found more frequently among the 91 infants who were lost to follow-up. The only positive predictor for postnatal follow-up was a prenatal consultation with the pediatric urologist. 1-4 The majority of these fetuses recover spontaneously but approximately 40% require postnatal follow-up, and in half of these cases, medical or surgical intervention was needed to prevent significant renal damage. The spectrum of genitourinary abnormalities detected antenatally is varied but the majority of patients have ANH.5 It is commonly accepted that no specific etiology can be identified in 48% of ANH cases.1-5 Physiologic changes are seen in 15%, ureteropelvic and ureterovesical junction obstructions account for 11% of the cases, 9% have vesicoureteral reflux, 4% have unilateral or bilateral megaloureters, 2% of all cases have multicystic dysplastic kidney (MCDK) and 1% have ureterocele. 1,3,6 Regardless of the cause, it is expected that about half of the ANH cases will resolve before delivery or during the first year of life. 2,6 For the other half there will be a need for postnatal follow-up as persistent uropathy is expected to occur in 12% of mild, 45% of moderate and 88% of severe ANH cases.

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Section: Discussionsupporting

confidence: 52%

Postnatal follow-up of antenatal hydronephrosis: a health-care challenge

et al. 2009

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“…Alternatively, urinary tract dilatation might occur normally during urinary tract development, perhaps due to the occurrence of VUR before the formation of a competent flap-valve mechanism. In reviewing the long-term follow-up of antenatal urinary tract dilatation, there are always some cases where previously observed abnormalities are no longer detected in the postnatal period (14,25). Our data suggest that in wild-type mice, VUR resolves in the newborn period because the flap-valve mechanism has now become competent.…”

Section: Discussionmentioning

confidence: 60%

“…Urinary tract dilatation discovered on antenatal ultrasounds is not always detected on postnatal imaging (14,25). This raises many questions regarding its natural history, including the possibility that dilatation can occur as a transient finding during normal human embryogenesis (20).…”

Section: Hoxb7/ret Mice Have a High Incidence Of Vur Hoxb7/retmentioning

confidence: 99%

Overexpression of RET leads to vesicoureteric reflux in mice

Murawski

Myburgh

et al. 2004

American Journal of Physiology-Renal Physiology

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, a tyrosine kinase receptor essential for kidney development, has recently been shown to be important for the formation of the urinary tract. When RET is overexpressed in the HoxB7/Ret transgenic mouse, kidneys are small and cystic, and in some of the mice, the ureters are grossly dilated. Here, we report that the observed ureteral dilatation is associated with the urinary tract abnormality vesicoureteric reflux (VUR), in which urine flows retrogradely from the bladder to the ureter. Reflux was determined in vitro by injecting methylene blue into the bladders of HoxB7/Ret and wild-type mice. At postnatal day 1, 30% of HoxB7/Ret mice had VUR compared with 4% of wild-type mice (P Ͻ 0.05). The length of the intravesical ureteral tunnel was shorter in HoxB7/Ret mice compared with wild-type mice, on both the right and the left sides (P Ͻ 0.05), suggesting a basis for the higher incidence of VUR in these mutants. At embryonic day 11, the ureteric bud was found to exit more caudally from the mesonephric duct in HoxB7/Ret mice, and this may predispose them to VUR (P Ͻ 0.05). Wild-type and HoxB7/Ret mice were tested for reflux at embryonic day 17, and both showed a high frequency of VUR (59 and 75%, respectively). These results suggest that VUR may occur transiently during normal urinary tract development before the ureter has completed its insertion into the bladder. In the HoxB7/Ret mouse, overexpression of RET appears to delay the maturation of the distal ureter, resulting in postnatal VUR. The HoxB7/Ret mouse is thus an important model in which to examine how vesicoureteric reflux arises during urinary tract development. kidney defect; urinary tract defect; ureteric bud PRIMARY VESICOURETERIC REFLUX (VUR) is a urinary tract abnormality in which urine flows retrogradely from the bladder to the ureters because of an anatomic defect at the junction of the ureter and the bladder. It affects 1-2% of children and predisposes them to recurrent urinary tract infections and in some cases, end-stage renal disease (7, 33). The condition is hereditary: it frequently affects multiple family members, and several genetic loci have been identified from linkage studies of affected families (5, 6).VUR is normally prevented by a functional valve, the flap-valve mechanism, that forms at the site of the ureteral insertion into the bladder. The flap-valve is dependent on 1) the tunnel in which the ureter enters into the bladder, 2) the presence of a muscular layer within the bladder and the ureter, and 3) the position of the ureteral orifice in the muscular layer within the bladder (the trigone). When the bladder is distended with urine, the tunnel is compressed, and this prevents the retrograde passage of urine from the bladder to the kidneys.The length of the intravesical ureteral tunnel is critical for the flap-valve mechanism: shorter tunnels have been identified in patients with VUR (17, 32). Other anatomic findings that have been associated with VUR include a lack of musculature within the ureter and its tunnel (30) and a ureteral ...

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“…Five hundred and six potentially relevant studies were identified, of which 18 met the inclusion criteria (17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). Two studies reported overlapping patient cohorts but different outcomes (27,28).…”

Section: Study Characteristicsmentioning

confidence: 99%

“…The earliest reported fetal ultrasound was at 14 wk of gestation (21). Most studies reported that postnatal scans were not performed within 2 d after birth (17,20,22,23,(27)(28)(29)(30)(31), which may be important because newborns are initially oliguric and false-negative results are common at this time: 4 studies did not specify the earliest age at postnatal ultrasound assessment (18,29,30,33).…”

Section: Study Characteristicsmentioning

confidence: 99%

Mild Fetal Renal Pelvis Dilatation—Much Ado About Nothing?

Hothi¹,

Wade²,

Gilbert³

et al. 2009

Clinical Journal of the American Society of Nephrology

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Background: Renal pelvis dilatation (RPD) occurs in 1% of fetuses. Severe RPD (>15 mm) is frequently associated with urinary tract pathology. For the majority with mild (5 to 9 mm) to moderate (10 to 15 mm) RPD, however, there is uncertainty about the risk of abnormalities and how much postnatal investigation is required.Study design: Systematic review of cohort studies of fetuses with RPD < 15 mm and metaregression to estimate risks of postnatal RPD, obstruction, and VUR.Results: Of 506 potentially relevant papers, 18 met the inclusion criteria. Risk of postnatal RPD increased with fetal RP size and earlier gestation. Odds ratios for postnatal RPD doubled per millimeter increase in fetal RP size: At 20 wk gestation, for example, 18% of fetuses with mean RP of 6 mm were estimated to have persistent postnatal RPD, compared with 95% of fetuses with 12 mm RPD, but risks were decreased by 16% to 18% per week of presentation gestation. Estimated risks of obstruction and VUR were substantially lower, particularly in the mild group such as the 6 mm example above: obstruction 2%, VUR 4%.Conclusions: Our novel risk estimates are useful for antenatal counseling at presentation. The low frequency of obstruction/ VUR in mild RPD raises questions over the most appropriate investigation of these cases but further data are required before establishing definitive postnatal management pathways. We suggest the need for a large prospective multicenter study to collect individual patient parameters/results and search for additional prognostic indicators.

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Postnatal Follow-Up of Hydronephrosis Detected by Prenatal Ultrasound: The Natural History

Cited by 54 publications

References 26 publications

Postnatal follow-up of antenatal hydronephrosis: a health-care challenge

Postnatal follow-up of antenatal hydronephrosis: a health-care challenge

Overexpression of RET leads to vesicoureteric reflux in mice

Mild Fetal Renal Pelvis Dilatation—Much Ado About Nothing?

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