Mild-to-moderate renal pelvis dilatation identified during pregnancy and hospital admissions in childhood: An electronic birth cohort study in Wales, UK.

BACKGROUND: Chronic kidney disease (CKD) is a growing contributor to the global burden of noncommunicable diseases. Early diagnosis and treatment can reduce the severity of kidney damage and the need for dialysis or transplantation. It is not known whether mild-to-moderate renal pelvis dilatation (RPD) identified at 18-20 weeks gestation is an early indicator of renal pathology. The aim of this follow-up to the Welsh Study of Mothers and Babies was to assess the risk of hospital admission in children with mild-to-moderate antenatal RPD compared with children without this finding. We also examined how the natural history of the RPD (whether the dilatation persists in later pregnancy or postpartum) or its characteristics (unilateral versus bilateral) changed the risk of hospital admission. METHODS/FINDINGS: This population-based cohort study included singleton babies born in Wales between January 1, 2009, and December 31, 2011 (n = 22,045). We linked ultrasound scan data to routinely available data on hospital admissions from the Patient Episode Database for Wales (PEDW). The outcome was a hospital admission for urinary tract causes (defined by an expert study steering group) in the first three years of life. We used Cox regression to model time to first hospital admission, according to whether there was evidence of RPD at the fetal anomaly scan (FAS) and/or evidence of dilatation in later investigations, adjusting for other predictors of admission. We used multiple imputation with chained equations to impute values for missing data. We included 21,239 children in the analysis. The risk of at least one hospital admission was seven times greater in those with RPD (n = 138) compared with those without (n = 21,101, conditional hazard ratio [cHR] 7.23, 95% confidence interval [CI] 4.31-12.15, p < 0.001). The risk of hospital admission was higher in children with RPD at the FAS and later dilatation (cHR 25.13, 95% CI 13.26-47.64, p < 0.001) and in children without RPD at the FAS who had later dilatation (cHR 62.06, 95% CI 41.10-93.71, p < 0.001) than in children without RPD (n = 21,057). Among children with RPD at the FAS but no dilatation in later pregnancy or postpartum, we did not find an association with hospital admissions (cHR 2.16, 95% CI 0.69-6.75, p = 0.185), except when the initial dilatation was bilateral (cHR 4.77, 95% CI 1.17-19.47, p = 0.029). Limitations of the study include small numbers in subgroups (meaning that these results should be interpreted with caution), that less severe outcomes (such as urinary tract infections [UTIs] managed in the community or in outpatients) could not be included in our analysis, and that obtaining records of radiological investigations later in pregnancy and postpartum was challenging. Our conclusions were consistent after conducting sensitivity analyses to account for some of these limitations. CONCLUSIONS: In this large population-based study, children with RPD at the FAS had higher rates of hospital admissions when there was persistent dilatation in later pregnancy or postpartum. Our results can be used to improve counselling of parents and develop care pathways for antenatal screening programmes, including protocols for reporting and further investigation of RPD.

Protein Kinase 2ß Is Expressed in Neural Crest-Derived Urinary Pacemaker Cells and Required for Pyeloureteric Contraction.

Nonobstructive hydronephrosis, defined as dilatation of the renal pelvis with or without dilatation of the ureter, is the most common antenatal abnormality detected by fetal ultrasound. Yet, the etiology of nonobstructive hydronephrosis is poorly defined. We previously demonstrated that defective development of urinary tract pacemaker cells (utPMCs) expressing hyperpolarization-activated cyclic nucleotide-gated channel 3 (HCN3) and the stem cell marker cKIT causes abnormal ureteric peristalsis and nonobstructive hydronephrosis. However, further investigation of utPMC development and function is limited by lack of knowledge regarding the embryonic derivation, development, and molecular apparatus of these cells. Here, we used lineage tracing in mice to identify cells that give rise to utPMCs. Neural crest cells (NCCs) indelibly labeled with tdTomato expressed HCN3 and cKIT. Furthermore, purified HCN3+ and cKIT+ utPMCs were enriched in Sox10 and Tfap-2α, markers of NCCs. Sequencing of purified RNA from HCN3+ cells revealed enrichment of a small subset of RNAs, including RNA encoding protein kinase 2ß (PTK2ß), a Ca2+-dependent tyrosine kinase that regulates ion channel activity in neurons. Immunofluorescence analysis in situ revealed PTK2ß expression in NCCs as early as embryonic day 12.5 and in HCN3+ and cKIT+ utPMCs as early as embryonic day 15.5, with sustained expression in HCN3+ utPMCs until postnatal week 8. Pharmacologic inhibition of PTK2ß in murine pyeloureteral tissue explants inhibited contraction frequency. Together, these results demonstrate that utPMCs are derived from NCCs, identify new markers of utPMCs, and demonstrate a functional contribution of PTK2ß to utPMC function.

Activated Hedgehog-GLI Signaling Causes Congenital Ureteropelvic Junction Obstruction.

Intrinsic ureteropelvic junction obstruction is the most common cause of congenital hydronephrosis, yet the underlying pathogenesis is undefined. Hedgehog proteins control morphogenesis by promoting GLI-dependent transcriptional activation and inhibiting the formation of the GLI3 transcriptional repressor. Hedgehog regulates differentiation and proliferation of ureteric smooth muscle progenitor cells during murine kidney-ureter development. Histopathologic findings of smooth muscle cell hypertrophy and stroma-like cells, consistently observed in obstructing tissue at the time of surgical correction, suggest that Hedgehog signaling is abnormally regulated during the genesis of congenital intrinsic ureteropelvic junction obstruction. Here, we demonstrate that constitutively active Hedgehog signaling in murine intermediate mesoderm-derived renal progenitors results in hydronephrosis and failure to develop a patent pelvic-ureteric junction. Tissue obstructing the ureteropelvic junction was marked as early as E13.5 by an ectopic population of cells expressing Ptch2, a Hedgehog signaling target. Constitutive expression of GLI3 repressor in Ptch1-deficient mice rescued ectopic Ptch2 expression and obstructive hydronephrosis. Whole transcriptome analysis of isolated Ptch2+ cells revealed coexpression of genes characteristic of stromal progenitor cells. Genetic lineage tracing indicated that stromal cells blocking the ureteropelvic junction were derived from intermediate mesoderm-derived renal progenitors and were distinct from the smooth muscle or epithelial lineages. Analysis of obstructive ureteric tissue resected from children with congenital intrinsic ureteropelvic junction obstruction revealed a molecular signature similar to that observed in Ptch1-deficient mice. Together, these results demonstrate a Hedgehog-dependent mechanism underlying mammalian intrinsic ureteropelvic junction obstruction.

Frequency of postnatal hydronephrosis in infants with a renal anterior-posterior pelvic diameter > 4 mm on midtrimester ultrasound.

OBJECTIVE: To examine the association of antenatal renal pelvic dilatation observed on midtrimester ultrasound screening with the presence of hydronephrosis in newborn infants. MATERIALS AND METHODS: The records of patients who received fetal ultrasound examination at 18-28 weeks' gestation from May 2008 to March 2012 were retrospectively reviewed. A fetal renal pelvic anterior-posterior (AP) diameter > 4 mm was considered abnormal and ≤ 4 mm was considered normal. On postnatal ultrasound, a renal pelvic AP diameter > 3 mm was considered to indicate hydronephrosis and ≤ 3 mm was considered normal. The association of postnatal hydronephrosis with prenatal pelvic AP diameter was determined using binary logistic regression analysis. RESULTS: The study comprised 1310 newborn infants: 684 (52.2%) male and 626 (47.8%) female. Multivariate analysis showed a right or left prenatal AP renal pelvic diameter > 4 mm was associated with a higher risk of postnatal hydronephrosis compared with a right and left prenatal AP renal pelvic diameter ≤ 4 mm. Boys had a higher risk for postnatal hydronephrosis than girls (odds ratio = 2.42, p < 0.05). CONCLUSION: An antenatal renal pelvic AP diameter > 4 mm on midtrimester ultrasound is predictive of postnatal hydronephrosis.

Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions.

Most cases of congenital obstructive nephropathy are the result of ureteropelvic junction obstructions, and despite their high prevalence, we have a poor understanding of their etiology and scarcity of genetic models. The eight-protein exocyst complex regulates polarized exocytosis of intracellular vesicles in a large variety of cell types. Here we report generation of a conditional knockout mouse for Sec10, a central component of the exocyst, which is the first conditional allele for any exocyst gene. Inactivation of Sec10 in ureteric bud-derived cells using Ksp1.3-Cre mice resulted in severe bilateral hydronephrosis and complete anuria in newborns, with death occurring 6-14 hours after birth. Sec10 FL/FL;Ksp-Cre embryos developed ureteropelvic junction obstructions between E17.5 and E18.5 as a result of degeneration of the urothelium and subsequent overgrowth by surrounding mesenchymal cells. The urothelial cell layer that lines the urinary tract must maintain a hydrophobic luminal barrier again urine while remaining highly stretchable. This barrier is largely established by production of uroplakin proteins that are transported to the apical surface to establish large plaques. By E16.5, Sec10 FL/FL;Ksp-Cre ureter and pelvic urothelium showed decreased uroplakin-3 protein at the luminal surface, and complete absence of uroplakin-3 by E17.5. Affected urothelium at the UPJ showed irregular barriers that exposed the smooth muscle layer to urine, suggesting this may trigger the surrounding mesenchymal cells to overgrow the lumen. Findings from this novel mouse model show Sec10 is critical for the development of the urothelium in ureters, and provides experimental evidence that failure of this urothelial barrier may contribute to human congenital urinary tract obstructions.

Expression of VEGF in neonatal urinary obstruction: does expression of VEGF predict hydronephrosis?

BACKGROUND: In animal studies, the inhibition of VEGF activity results in high mortality and impaired renal and glomerular development. Mechanical stimuli, like mechanical stretch in respiratory and circulatory systems, results in an elevated expression of VEGF. In animal models, the experimental urinary obstruction is associated with stretching of tubular cells and activations of the renin-angiotensin system. This results in the upregulation of vascular endothelial growth factor (VEGF) and TNF-alfa. MATERIAL/METHODS: Tissue samples from urinary tract obstruction were collected and immunohistochemistry was performed in 14 patients (average age: 7.1±4.1 years). The control histology group consisted of ureteropelvic junction tissue from 10 fetuses after midtrimester artificial abortion. The fetuses did not have any failure at ultrasound screening and pathological examination. The mean gestational age was 20.6 weeks of gestation (±2.2SD). Expression of VEGF was detected with immunohistochemistry method. RESULTS: Expression of VEGF was found in varying intensity in the submucosa and subserosa layers, but only in the test tissue (placental tissue). The tissue of the patients with urinary obstruction and the tissue of the fetal ureteropelvic junction without urinary obstruction were negative for expression of VEGF. The repeated examination showed negative cells and no color staining. CONCLUSIONS: The pressure due to congenital urogenital obstruction resulting in mechanical stress in cells did not increase the expression of VEGF in young children in our study. To find a correlation between urogenital tract obstruction and increased expression of VEGF, we need to perform more examinations because the connection may be of therapeutic significance.

Size and volume charts of fetal kidney, renal pelvis and adrenal gland.

OBJECTIVE: To establish reference curves for size and volume of the fetal kidney, renal pelvis and adrenal gland, as measured using ultrasound from the 15(th) week of gestation. METHODS: This was a prospective, longitudinal study of 96 fetuses in low-risk singleton pregnancies, in which we performed serial ultrasound examinations at 4-week intervals. The length and anteroposterior and transverse diameters of both kidneys, the anteroposterior and transverse diameters of the renal pelvises and the length of the adrenal glands were measured three times at each examination, with the average being used for further analysis. Reference charts were constructed using multilevel statistical analysis and comparisons were made with previously published charts derived from cross-sectional data. RESULTS: We present nomograms for fetal kidney dimensions and volume, renal pelvis dimensions and adrenal gland length. The new charts show differences in shape and have narrower percentile bands in comparison to previously published reference ranges. CONCLUSIONS: These new charts of measurements of the fetal kidney, renal pelvis and adrenal gland, from a prospective, longitudinal study, may be useful in the diagnosis and assessment of pathology of the kidney and adrenal gland.

Postnatal outcome of prenatally diagnosed severe fetal renal pelvic dilatation.

OBJECTIVE: We correlated the prenatal severity with the postnatal outcome of prenatally detected renal pelvic dilatation (RPD). METHODS: Cases of prenatally detected RPD referred between January 2002 and December 2008 were included. Severe RPD was defined as an anterior-posterior diameter of 15 mm, mild and moderate dilatation was defined as 6 to <10 mm and 10 to <15 mm, respectively. Postnatal diagnosis, the need for surgery and the correlation with the prenatal severity was ascertained. RESULTS: Of the 762 patients with RPD, 492 (64.5%) were mild, 167 (21.9%) were moderate, and 103 (13.5%) were severe. The male:female ratio for the severe cohort was 5:1. Of the sever cases, 68% had progressive dilatation. Of the mild/moderate cases, 5% progressed to severe dilatation. PUJ obstruction was confirmed in 48 cases (60.8%), severe VUR in 11 cases (14%), VUJ obstruction in 5 cases (6%), PUV in 2 cases (2.5%), and a nonidentifiable cause in 13 cases (16.5%). Ten of the 48 (20.8%) babies with PUJ obstruction required surgery within the first year of life. CONCLUSION: An obstructive cause is usually present in severe cases, which are more likely to require surgery if there is PUJ obstruction. A high male:female ratio was present in this group.

Diagnostic value of anteroposterior diameter of fetal renal pelvis during second and third trimesters in predicting postnatal surgery among Korean population: useful information for antenatal counseling.

OBJECTIVE: To establish prognostic data regarding fetal hydronephrosis using the anteroposterior diameter (APD) and the need for interventional surgery in the Korean population. METHODS: A total of 187 children with an APD of ≥ 4 mm on obstetric ultrasound scans at any gestational age were retrospectively reviewed. The affected renal units were divided into 2 groups: surgical and nonsurgical. The ultrasound findings were compared at 3 gestational ages: second trimester (15-26 weeks' gestation), early third trimester (27-33 weeks' gestation), and late third trimester (34-40 weeks' gestation). RESULTS: The area under the receiver operating characteristic curve was 0.770, 0.828, and 0.812 at the second, early third, and late third trimesters, respectively. A 100% sensitivity for predicting postnatal surgery could be achieved at a cutoff APD of 5 mm during the second trimester, 8 mm during the early third trimester, and 10 mm during the late third trimester if scheduled antenatal ultrasound scans were performed. A cutoff APD of 11 mm during the second trimester was of diagnostic value in selecting children at risk of postnatal surgery with an odds ratio of 5.13 (95% confidence interval 1.62-16.25), with relatively high sensitivity and specificity. With a cutoff of 15 mm during the early third and late third trimesters, the odds ratio was 11.51 (95% confidence interval 5.05-26.23) and 6.94 (95% confidence interval 3.30-14.57), respectively. CONCLUSION: Compared with an APD of 10 mm, the most commonly used standard cutoff value in predicting postnatal hydronephrosis and its outcome, an APD cutoff of 5, 8, and 10 mm during the second, early third, and late third trimesters, respectively, is more specific in predicting the need for postnatal surgical intervention in the Korean population.

Absence of canonical Smad signaling in ureteral and bladder mesenchyme causes ureteropelvic junction obstruction.

Obstruction of the ureteropelvic junction (UPJ) is a common congenital anomaly frequently associated with ureteral defects. To study the molecular mechanisms that modulate ureteral development, we inactivated Smad4, the common Smad critical for transcriptional responses to TGF-ß and Bmp signaling, in the ureteral and bladder mesenchyme during embryogenesis. Loss of canonical Smad signaling in these tissues caused bilateral UPJ obstruction and severe hydronephrosis beginning at embryonic day 17.5. Despite a reduction in quantity of ureteral smooth muscle, differentiation proceeded without Smad4, producing a less severe phenotype than Bmp4 mutants; this finding suggests that at least some Bmp4 functions in ureteral smooth muscle may be Smad-independent. The absence of canonical Smad signaling in the ureteral mesenchyme, but not in the urothelium itself, led to urothelial disorganization, highlighting the importance of mesenchymal support for epithelial development. Transcript profiling revealed altered expression in known Bmp targets, smooth muscle-specific genes, and extracellular matrix-related genes in mutant ureters before the onset of hydronephrosis. Expression of the Bmp target Id2 was significantly lower in Smad4 mutants, consistent with the observation that Id2 mutants develop UPJ obstruction. In summary, Smad4 deficiency reduces the number and contractility of ureteral smooth muscle cells, leading to abnormal pyeloureteral peristalsis and functional obstruction. The subsequent bending and luminal constriction of the ureter at the UPJ marks the transition from a functional obstruction to a more intractable physical obstruction, suggesting that early intervention for this disease may prevent more irreversible damage to the urinary tract.

Renal pelvic diameters in human fetuses: anatomical reference for diagnosis of fetal hydronephrosis.

OBJECTIVE: To evaluate renal pelvis diameters in human fetuses, to establish normative patterns of their growth and size during the second gestational trimester. METHODS: We studied 140 kidneys (70 fetuses; 38 male, 32 female) ranging in age from 12-25 weeks' postconception. The renal pelvis was dissected and the transverse and longitudinal diameters were measured. The renal length, width, and thickness were assessed. To compare the quantitative data in both sexes, Student's t-test was used (P <.05). RESULTS: The mean transverse diameter in male fetuses was 3.61 mm in the right side and 3.58 mm in the left. In female fetuses, it was 3.51 mm in the right side and 3.43 mm in the left. There was no statistical significant difference between the sides either in males (P <.81) or in females (P <.33). There was no significant difference in the mean transverse diameter between male and female fetuses (P <.9). The mean longitudinal diameter in male fetuses was 4.28 mm in the right side and 4.31 mm in the left. In female fetuses, it was 4.17 mm in the right side and 4.33 mm in the left. There was no significant statistical difference between the sides in either males (P <.82) or females (P <.33). There was no significant difference in the mean longitudinal diameter between male and female fetuses (P <.9). CONCLUSIONS: Transverse and longitudinal diameters are useful as parameters for assessment of the renal pelvis in human fetuses.

Ectasia piélica en diagnóstico prenata / Pyelic ectasia in prenatal diagnosis

La ecografía gestacional demuestra que el 1,4% de los fetos presentan algún grado de hidronefrosis, aunque en el 50%, dicha ectasia habrá desaparecido en el nacimiento. El desconocimiento que aún existe con respecto a las diferentes etapas del desarrollo fetal hace que sea difícil distinguir entre aquellas situaciones fisiológicas y las que son patológicas. La medición de los diámetros de la pelvis renal a lo largo de la gestación y la cantidad de líquido amniótico son datos importantes para establecer un pronóstico. Las válvulas de uretra posterior son las responsables de un buen número de casos de hidronefrosis gestacional significativa. Es importante diagnosticarlas y proceder a su tratamiento para evitar daño renal. Se presenta un caso clínico y se realiza una revisión sobre el tema proponiendo un algoritmo de actuación clínica (AU)

Gestational ultrasound shows that 1.4% of the fetuses have some degree of hydronephrosis, although in 50% renal ectasia will have disappeared at birth. The ignorance that still exists in the different stages of fetal development makes it difficult to distinguish between those situations that are physiological or pathological condition. Measuring the diameter of the renal pelvis throughout pregnancy and amniotic fluid are important data for establishing a prognosis. Posterior urethral valves are responsible for a number of significant cases of gestational hydronephrosis. It is important to diagnose it and provide treatment to prevent kidney damage. We present a case report and a review is made on the issue and we propos an algorithm for clinical intervention (AU)

[Stenosis of the upper renal pelvis: rare complication of an incomplete ureteral duplicity. Embryological investigation]. / La sténose du pyélon supérieur : complication rare d'une bifidité urétérale. Enquête embryologique.

A stenosis of the upper pole of an incomplete renal duplication is presented. The prenatal diagnosis of a right renal ureteropyelic junction syndrome, isolated, with a normal amniotic liquid was confirmed at birth. Intravenous pyelogram 8 days after birth showed three right dilated calical groups with a dilated renal ureteropyelic junction, but an normal inferior calical group suspected a renal bifidity. Renal MagIII scintigraphy evaluated the anatomical and functional stenosis and indicated surgery. Postoperative followings were simple and results good 3 years after. From this rare case, embryogenesis is discussed.

Diagnostic accuracy of postnatal ultrasound screening for urinary tract abnormalities.

The study was aimed at (1) the determination of the incidence of abnormalities of the urinary tract in newborn infants detected by postnatal ultrasound screening, and (2) the evaluation of the diagnostic accuracy of postnatal ultrasound screening for detecting surgical urinary tract abnormalities. The prospective study was of full-term neonates born in the University Hospital of Olomouc in 2005-2008 who underwent renal ultrasound screening after 72 h of life. Significant findings were recorded. Subsequent diagnostic and therapeutic procedures were recorded and evaluated in a group of children with detected renal pelvic dilatation (RPD). (1) A total of 6,088 newborn infants was examined. The absolute and relative RPD incidence rates (anteroposterior diameter, APD) were as follows: 5-7 mm, 146 (2.4%); 7-10 mm, 70 (1.15%); 10-15 mm, 13 (0.21%), and 15 mm or more, 5 (0.08%). Of those, 16 children were operated on for abnormalities of the urinary tract, of which nine (56%) had been detected by prenatal screening. Other findings: six cases of unilateral renal agenesis, four cases of multicystic renal dysplasia, four of renal dystopia, one of polycystic kidney disease and one of renal hypoplasia. (2) A group of 224 children with postnatally detected RPD was examined, of whom 40 (17.9%) underwent voiding cystourethrography and/or scintigraphy and 16 (7.1%) were treated surgically. The receiver operating characteristic curves were analyzed, and the areas under the curves were calculated. Postnatal renal ultrasound screening is probably a suitable test for detecting significant urinary tract abnormalities.

Antagonism of BMP4 signaling disrupts smooth muscle investment of the ureter and ureteropelvic junction.

PURPOSE: Congenital ureteropelvic junction obstruction has been associated with aberrant ureteral smooth muscle organization. Recent evidence has shown that BMP4 may be involved in ureteral morphogenesis. We determined whether the disruption of BMP4 signaling results in abnormal smooth muscle investment of the ureter and ureteropelvic junction. MATERIALS AND METHODS: We used a Cre mediated Bmp4 knockout system to conditionally excise the Bmp4 gene in developing mouse embryos. Kidney rudiments were isolated from embryos at varying gestational ages from WT and conditional knockout mice. Metanephric kidney explants were cultured in the presence or absence of the BMP antagonist Noggin. Agarose beads pre-incubated with Gremlin, another BMP antagonist, were used for localized disruption of BMP signaling. Frozen sections and whole metanephric explants were then analyzed by immunofluorescence. RESULTS: Bmp4 gene excision resulted in a dose dependent loss of ureteral smooth muscle. Antagonism of BMP signaling inhibited ureteral smooth muscle investment in a dose dependent manner and was paralleled by a dose dependent decrease in the immediate downstream targets of BMP signaling, phosphorylated Smad1, 5 and 8. Localized antagonism of BMP resulted in the focal disruption of ureteral smooth muscle investment. CONCLUSIONS: We report that decreased BMP signaling, whether by the loss of BMP4 in vivo or direct antagonism in vitro, results in a gradual reduction of the normal, well organized coat of smooth muscle surrounding the ureter. Our results also suggest that this occurs via a direct Smad dependent pathway. This raises the possibility that abnormalities in BMP4 signaling may have a role in the development of congenital ureteropelvic junction obstruction.

Hydronephrosis index: a better physiological reference in antenatal ultrasound for assessment of fetal hydronephrosis.

OBJECTIVE: To establish a nomogram of fetal hydronephrosis index (HI) (anteroposterior diameter of renal pelvis divided by urinary bladder volume) at different gestational ages, to serve as a new reference for antenatal ultrasound examination, and to avoid overestimation of fetal hydronephrosis due to transient effect of a distended fetal bladder. STUDY DESIGN: 504 uncomplicated singleton pregnancies from 20 to 38 weeks' gestation were included. In each fetus, the maximum anteroposterior diameters of both renal pelves were measured on transverse view of fetal kidneys. Urinary bladder volume was calculated using the ovoid volume formula. HI was derived accordingly. RESULTS: Values of HI vary significantly at different trimesters of pregnancy. HI was much higher (mean = 0.1543) from 20 to 27 weeks' gestation, and its value decreased significantly (mean = 0.0253) from 28 to 38 weeks' gestation (P < .05, independent-sample t test). As gestational age increased, HI decreased (R(2) = 0.5921). CONCLUSIONS: HI is easy to be measured and can be used as a new physiological reference for assessment of fetal hydronephrosis by eliminating the confounding effect of a full fetal bladder. The change in values of HI throughout gestation supports the clinical importance of a nomogram for this new index.

Mild fetal renal pelvis dilatation: much ado about nothing?

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 < or = 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.

Correlation of prenatal and postnatal ultrasound findings with the incidence of vesicoureteral reflux in children with fetal renal pelvic dilatation.

PURPOSE: Up to 1% of prenatal ultrasounds detect renal pelvic dilatation. This dilatation is associated with vesicoureteral reflux but its clinical significance and the necessity for vesicoureteral reflux detection have been questioned. We report an evaluation of fetal renal pelvic dilatation and postnatal sonographic features with the incidence of vesicoureteral reflux. MATERIALS AND METHODS: Maximum fetal renal pelvic dilatation was prospectively measured at a single center between 1990 and 2003. Dilatation 4 mm or greater at less than 33 weeks of gestation, or 7 mm or greater at more than 33 weeks was the threshold for inclusion in the study. Postnatal evaluation included ultrasound and voiding cystourethrogram. Postnatal data included vesicoureteral reflux incidence and grade, and caliceal and ureteral dilatation on ultrasound. RESULTS: Of 215 neonates 46 (21%) had vesicoureteral reflux. Mean renal pelvic dilatation was 14.4 mm in those with reflux, which was not statistically different than the mean of 11.8 mm in 169 with a normal voiding cystourethrogram. ROC analysis revealed that fetal renal pelvic dilatation was a poor discriminator of reflux. Reflux was identified in a significantly greater number of neonates with vs without postnatal calicectasis (20% vs 9%, p <0.05). When fetal renal pelvic dilatation was combined with postnatal calicectasis, only 5% of infants with dilatation less than 10 mm and isolated renal pelvic dilatation had reflux, whereas reflux was identified in 25% with fetal renal pelvic dilatation 10 mm or greater and calicectasis (p <0.02). CONCLUSIONS: The magnitude of fetal renal pelvic dilatation is not reliably predictive of reflux and this measure alone cannot be used to direct postnatal cystography. However, postnatal calicectasis appears to be an important predictor of vesicoureteral reflux in children with fetal renal pelvic dilatation. Expectant management can be considered in the subset of newborns with minimal dilatation (less than 10 mm) and absent calicectasis.