Fetal renal artery flow and renal echogenicity in the chronically hypoxic state

The object of this study was to investigate the fetal renal arterial blood flow in normal and hyperechogenic kidneys during the third trimester of gestation. The pregnancies screened were all chronically hypoxic. Depending on the etiology of the intrauterine chronic hypoxia, the cases were divided into two study groups. Group I comprised 120 pregnant women with pregnancy-associated hypertension and/or proteinuria. Group II consisted of 87 pregnancies with intrauterine growth retardation. Both study groups included pregnant women from the third trimester. Hyperechogenic renal medullae were detected in 15 out of 120 cases with pregnancy-associated hypertension and/or proteinuria, and in 22 fetuses of the 87 pregnancies involving intrauterine growth retardation. Fetal renal hyperechogenicity appears to be an indicator of fetal arterial circulatory depression, correlated with pathological changes in the resistance index for the fetal renal arteries. The fetal renal arterial blood flow resistance index was significantly lower in hyperechogenic cases. This may also be an in utero indication of subsequent intrauterine and neonatal complications, such as cesarean section because of fetal distress (43%), treatment in a neonatal intensive care unit (51%) or increased perinatal mortality (5.4%, as compared with 0.8–1.0% in the normal population). Detailed ultrasound and Doppler examinations of renal parenchyma and arteries appear to be useful methods in the prenatal diagnosis of reduced renal perfusion and of intrauterine hypoxia to detect possible pathological fetal conditions in utero. Received: 2 September 1998 / Revised: 5 May 1999 / Accepted: 7 May 1999     

What is biparietal diameter/kidney length ratio in cases with renal hyperechogenicity?

The object of this study was to investigate the fetal biparietal diameter/kidney length ratio in normal and hyperechogenic kidneys during the 3rd trimester of gestation. Screened pregnancies were chronically hypoxic [i.e. intrauterine growth retardation (IUGR)]. Depending on the renal manifestation of the intrauterine chronic hypoxia, the cases were divided into two study groups. Group I was composed of 28 fetuses with IUGR and hyperechogenic renal medullae. Group II consisted of 62 fetuses with IUGR and normal echoic kidney. Both study groups included pregnant women from the 3rd trimester. Fetal renal hyperechogenicity is an indicator of depression of fetal renal perfusion, correlated with pathological growth in the fetal kidney development. The fetal biparietal diameter/kidney length ratio was significantly higher in hyperechogenic cases. This may also be an in utero indicator of subsequent intrauterine and neonatal complications. Detailed ultrasound examinations of renal parenchyma and length appear to be useful in the prenatal diagnosis of reduced renal perfusion and of intrauterine hypoxia, allowing detection of possible pathological fetal conditions in utero.     

Vesicoamniotic shunt for complete urinary tract obstruction is partially effective

Purpose

The long-term outcome for children after antenatal intervention for obstructive uropathies is disappointing. We reported that renal dysplastic changes are well established 3 weeks after obstruction in a fetal lamb model. We used this model to explore renal development and bladder function after fetal intervention.

Methods

We created an obstructive uropathy in fetal lambs at 60 days gestation by ligating the urethra and urachus. A vesicostomy (female) or urethrostomy (male) were performed 21 days later. The fetuses were killed at term (145 days) and bladder volume and compliance were measured. The urinary tract was processed for histologic examination.

Results

Twenty two fetuses were shunted. Nine were miscarried or were still-born. Thirteen survived, and 11 had a successful shunt with a small bladder (8 ± 5 mL) compared with controls (71 ± 19 mL) (P < .05). Shunted bladders had poor compliance. Histologically, they had thickened submucosal connective tissue with hypertrophied muscle. Histology of the renal tissue demonstrated relatively well-preserved renal architecture with reduced nephron mass (oligonephronia) in 2 lambs and multicystic dysplastic change in 3. Six (55%) had normal nephrogenesis.

Conclusions

In our model, shunt operations after obstructive uropathy fail to preserve bladder function. Shunting ameliorated the development of cystic dysplasia, but half of the lambs had oligonephronia or multicystic dysplastic kidney. These might develop renal failure later in life.     

Compensatory renal growth due to neonatal ureteral obstruction: implications for clinical studies

In response to unilateral ureteral obstruction (UUO), the contralateral kidney undergoes compensatory renal growth, which is enhanced in early development. We investigated the renal growth response to UUO in the neonatal rat. Within 2 days of birth, animals were subjected to sham-operation, complete UUO, or variable partial UUO, and kidneys were harvested 3–60 days later. Contralateral kidney weight increased after only 7 days of complete UUO. Increase in contralateral kidney weight was not significant for partial UUO until 45 days, but kidney/body weight ratio increased after only 14 days of 0.3 mm partial UUO. The rate of contralateral renal growth increased with age and with increasing severity of UUO. In rats subjected to 45 days UUO, glomerular area was proportional to kidney/body weight ratio (r =0.61, p <0.01). We conclude that the rate of compensatory renal growth is dependent on the severity and duration of obstruction, and takes place at the single nephron level. The results suggest that biologic variability limits the early detection of compensatory renal growth, which is compounded by limitations in measuring renal size by clinical imaging. Factoring kidney length (or volume) by intervertebral length (or body surface area) should improve the precision of tracking renal growth.     

Study of the fetal kidney length growth during the second and third trimesters of gestation

The fetal kidney length growth was studied in 240 kidneys taken from 120 staged human fetuses (74 males and 46 females) ranging in age from 10 to 36 weeks postconception. Each kidney was quantitatively evaluated considering its greatest longitudinal length. The data were correlated to the gestational age by using the allometric method (Y = bXk). Equations and growth curves of right and left kidneys, males, females and the whole sample during the second and the third trimesters are presented. This study has practical utility in the quantitative determination of the renal anomalies and in the determination of the gestational age.     

Renal function following kidney transplantation in children treated with cyclosporine

The study was performed to evaluate the longterm renal function of children treated with cyclosporine after kidney transplantation. Renal function was determined with clearances of inulin and aminohippurate sodium for evaluating glomerular filtration rate (GFR) and effective renal plasma flow (ERPF). Thirty-six children aged 0.4–16.2 (median 6.9) years at transplantation were examined within 5 months of transplantation and then yearly over 0.3–7.1 years. Twenty-five children and young adults, 1.5–20 (median 7.7) years of age, with solitary kidneys because of renal agenesis or nephrectomy, served as controls. The GFR and ERPF within 1 year of transplantation were significantly lower than those of controls (65±19 and 345±88 vs 96±12 and 474±91 ml/min per 1.73 m², respectively). GFR remained constant 4 years after transplantation, but ERPF decreased significantly. Significant inverse correlations were found between GFR within 5 months of transplantation and the mean cyclosporine concentration and the number of rejection episodes. The frequency of hypertension decreased from 82% within 5 months of transplantation to 0% after 4 years. The absolute GFR increased during follow-up. In conclusion, kidney transplantation results in a reduced renal function compared with that of solitary native kidneys. The reduction in renal function correlated with the number of rejection episodes and the cyclosporine load. The increase in absolute GFR during follow-up suggests a remaining capacity for growth and/or compensatory hypertrophy.     

Fetal and Infant Growth Patterns and Kidney Function at School Age

Low birth weight is associated with ESRD. To identify specific growth patterns in early life that may be related to kidney function in later life, we examined the associations of longitudinally measured fetal and infant growth with kidney function in school-aged children. This study was embedded in a population-based prospective cohort study among 6482 children followed from fetal life onward. Fetal and childhood growth was measured during second and third trimesters of pregnancy, at birth, and at 6, 12, 24, 36, and 48 months postnatally. At the age of 6 years, we measured kidney volume by ultrasound. GFR was estimated using blood creatinine levels. Higher gestational age-adjusted birth weight was associated with higher combined kidney volume and higher eGFR (per 1 SD score increase in birth weight; 1.27 cm³ [95% confidence interval, 0.61 to 1.93] and 0.78 ml/min per 1.73 m² [95% CI, 0.16 to 1.39], respectively). Fetal weight, birth weight, and weight at 6 months were positively associated with childhood kidney volume, whereas higher second trimester fetal weight was positively associated with higher GFR (all P values<0.05). Fetal and childhood lengths were not consistently associated with kidney function. In this cohort, lower fetal and early infant weight growth is associated with smaller kidney volume in childhood, whereas only lower fetal weight growth is associated with lower kidney function in childhood, independent of childhood growth. Whether these associations lead to an increased risk of kidney disease needs to be studied further.Low birth weight is associated with higher risks of ESRD and hypertension in later life.^1–3 Clearly, low birth weight is not the causal factor per se leading to kidney diseases in later life. Birth weight is the result of various exposures and growth patterns in fetal life and the starting point of childhood growth. It has been hypothesized that especially third trimester fetal growth restriction leads to persistently smaller kidneys with a reduced number of nephrons, which may predispose the individual to kidney disease in adulthood.^4–6 This hypothesis is supported by both animal and human studies, showing that kidney volume and nephron number are reduced in fetal growth-restricted subjects and hypertensive subjects.^7–9 Although nephrogenesis is known to continue until 36 weeks of gestation and cease thereafter, not much is known about the specific critical periods and early growth patterns related to kidney function in later life.¹⁰ Also, whether and to what extent the associations of low birth weight with CKD are explained by preterm birth are not known.¹ Longitudinal studies suggested that the associations of low birth weight with hypertension were stronger in subjects with rapid weight gain in childhood, but results are inconclusive.^11,12 A similar growth pattern has not been identified as a risk factor for kidney diseases yet.Prospective studies linking fetal and early childhood growth patterns to kidney outcomes in later life might help to identify early critical periods for developing impaired kidney function in later life.Therefore, we examined, in a population-based prospective cohort study among 6482 children followed from early fetal life onward (Figure 1), the associations of birth weight, gestational age, birth weight for gestational age, and longitudinally measured fetal and early childhood growth patterns with kidney size and function at school age. We used subclinical variations of kidney function in childhood as outcomes, because they relate to kidney disease in later life.¹³Open in a separate windowFigure 1.Flow chart: exclusion criteria and numbers of participants are given. Total numbers of available outcome measurements are given.     

Fetal renal hyperechogenicity in intrauterine growth retardation: importance and outcome

The object of the study was to investigate the outcome in growth-retarded newborns who were diagnosed with fetal renal hyperechogenicity without anatomical abnormality during any stage of pregnancy. Depending on the fetal renal ultrasonography result, the cases were divided into two study groups. There was an intrauterine growth-retarded group with fetal renal medullary hyperechogenicity and another group without fetal renal medullary hyperechogenicity. The renal parenchyma was observed after birth, within the first 5 days of life, and several times until the 14thpostpartum day in positive cases. Hyperechogenic renal medullae were detected in 25 of 90 cases with intrauterine growth retardation during the 8-month study period. This may be an in utero cause of subsequent intrauterine and neonatal complications, such as cesarean section because of fetal distress (36%), perinatal infection (24%), treatment in a neonatal intensive care unit (52%), or increased perinatal mortality (8%). The results demonstrate that fetuses with hyperechoic medullae had 1.5 times the risk of an abnormal outcome compared with fetuses with normal echoic kidneys and intrauterine growth retardation. Detailed ultrasound examinations of renal parenchyma appear to be useful for the prenatal diagnosis of intrauterine hypoxia, allowing the detection of possible pathological fetal conditions in utero. Received: 2 November 1999 / Revised: 1 February 2001 / Accepted: 7 February 2001     

Prenatal diagnosis and outcome of fetal lung masses

Aim

The purpose of this study is to evaluate the accuracy of prenatal diagnostic features, particularly congenital cystic adenomatoid malformation volume ratio (CVR), in predicting outcomes for fetuses with lung masses.

Methods

The records and imaging features of all fetuses referred to the Texas Children's Fetal Center with a fetal lung mass between July 2001 and May 2010 were reviewed retrospectively. Data collected included gestational age (GA) at diagnosis, fetal magnetic resonance imaging findings, CVR, mass size, nature of fetal treatment, surgical findings, pathology, and outcome. Data were analyzed for predicting development of hydrops or the need for fetal therapy using receiver operating characteristic curves.

Results

Of 82 fetuses (41 male) evaluated for a lung mass, 53 (65%) were left-sided (1 bilateral), and the mean (SD) GA at diagnosis was 21.5 (4.3) weeks. Seventy-three fetuses underwent fetal magnetic resonance imaging at a mean (SD) GA of 26.1 (4.6) weeks. Thirteen fetuses (16%) had fetal treatment. Four fetuses with hydrops underwent open fetal surgical resection, and 3 survived. Six fetuses with large lung masses and persistent mediastinal compression near term underwent ex-utero intrapartum therapy-to-resection procedures, and 3 fetuses with hydrops underwent serial thoracentesis. Congenital cystic adenomatoid malformation volume ratio correlated strongly with the development of hydrops and the need for fetal therapy with an area under the receiver operating characteristic curve of 0.96 (P < .0001) and 0.88 (P < .0001), respectively. Of 18 fetuses with a CVR greater than 2.0 compared with 2 (3%) of 60 with a CVR of 2.0 or less, 10 (56%) required fetal intervention (P < .0001).

Conclusion

Congenital cystic adenomatoid malformation volume ratio correlates strongly with the development of fetal hydrops and the need for fetal intervention. A threshold value of 2.0 yields the most powerful statistical results.     

Spleen's relative growth in human fetuses.

The growth of the spleen weight was studied by bivariate allometry. It was correlated to fetal parameters of development as gestational age (in weeks), crown-rump length (mm) and weight (gm). Thirty human fetuses ranging from 16 to 36 weeks were studied. These were analysed in second and third trimesters separately and together. The growth of the spleen weight presents statistically significant positive allometry relative to age, C-R length and fetal weight. In second trimester the allometric coefficient, analysing spleen's weight and fetus' weight, calculated by reduced major axis method (RMA) was 1.21. In the third one the RMA was 1.73. Considering fetuses together the RMA = 1.65. This study presents growth curves of the spleen weight useful in medical branches such as anatomy, forensic medicine, medical imagery, fetophatology, obstetrics and pediatrics.     

Maternal smoking during pregnancy and kidney volume in the offspring: the Generation R Study

An adverse fetal environment leads to smaller kidneys, with fewer nephrons, which might predispose an individual to the development of kidney disease and hypertension in adult life. In a prospective cohort study among 1,072 children followed from early fetal life onward, we examined whether maternal smoking during pregnancy, as a significant adverse fetal exposure, is associated with fetal (third trimester of pregnancy, n = 1,031) and infant kidney volume (2 years of age, n = 538) measured by ultrasound. Analyses were adjusted for various potential confounders. Among mothers who continued smoking, we observed dose-dependent associations between the number of cigarettes smoked during pregnancy and kidney volume in fetal life. Smoking less than five cigarettes per day was associated with larger fetal combined kidney volume, while smoking more than ten cigarettes per day tended to be associated with smaller fetal combined kidney volume (p for trend: 0.002). This pattern was not significant for kidney volume at the age of 2 years. Our results suggest that smoking during pregnancy might affect kidney development in fetal life with a dose-dependent relationship. Further studies are needed to assess the underlying mechanisms and whether these differences in fetal kidney volume have postnatal consequences for kidney function and blood pressure.     

Childhood Kidney Outcomes in Relation to Fetal Blood Flow and Kidney Size

Impaired fetal abdominal blood flow may lead to smaller kidneys and subsequent impaired kidney function in later life. In a prospective cohort study among 923 pregnant women and their children, we measured fetal growth, kidney volumes, and umbilical and cerebral artery blood flow (median gestational age of 30.3 weeks; 95% range, 28.5–32.7 weeks). We used a higher umbilical/cerebral artery pulsatility index ratio as an indicator of preferential fetal blood flow to the upper body parts at the expense of the intra-abdominal organs. At a median age of 5.9 years (95% range, 5.7–6.6 years), we measured childhood kidney volumes, creatinine and cystatin C blood levels, microalbuminuria, BP, and eGFR. A preferential fetal blood flow to the upper body parts at the expense of the intra-abdominal organs associated only with a smaller combined kidney volume in childhood. Fetal combined kidney volume positively associated with childhood combined kidney volume and eGFR, and inversely associated with childhood creatinine and cystatin C levels (all P values <0.05), but did not associate with childhood microalbuminuria and BP. Children within the highest tertile of fetal umbilical/cerebral ratio and the lowest tertile of fetal combined kidney volume had the lowest eGFR (difference, −6.36 ml/min per 1.73 m²; 95% confidence interval, −11.78 to −0.94 compared with children within the middle tertiles). These data suggest that impaired fetal blood to the abdominal organs and smaller fetal kidney size are associated with subclinical changes in kidney outcomes in school-aged children.The third trimester of pregnancy is a critical period for fetal kidney development.¹ Nephrogenesis continues until 36 weeks of gestation, after which the induction of nephron numbers ceases.² A permanent reduction of kidney size and number of nephrons leads to a smaller glomerular filtration surface area, which might predispose the individual to decreased kidney function in childhood and subsequently to kidney disease and hypertension in adulthood.^3,4 This hypothesis is supported by studies showing consistent associations of low birth weight with higher risks of kidney disease and hypertension in later life.^5,6 Although the observed effect estimates from these studies were small, they are important from an etiologic perspective.^5,6 In addition, post mortem studies showed that the nephron number is lower in hypertensive individuals than in normotensive controls⁷ and is positively correlated with birth weight and kidney size.^8,9 Animal studies demonstrated a reduction in nephron number as a result of vascular placental insufficiency.¹⁰ Placental insufficiency is an important risk factor for fetal growth restriction and low birth weight.¹¹ We recently demonstrated that increased third trimester placental insufficiency is associated with a higher BP in childhood.¹² Placental insufficiency is characterized by a preferential fetal blood flow to the brain at the expense of the trunk.¹³ This fetal blood flow redistribution is caused by higher peripheral and lower cerebral arterial resistance,¹¹ and can be measured as a higher umbilical artery pulsatility index (PI) and lower cerebral artery PI, respectively. This combination leads to a higher ratio of these measures (higher umbilical/cerebral (U/C) ratio).¹⁴ It is unknown whether and to what extent impaired abdominal or kidney blood flow and kidney growth restriction during fetal life lead to risk factors for kidney disease in later life.In this population-based prospective cohort study among 923 pregnant women and their children, we evaluated the associations of third trimester fetal blood flow redistribution, at the expense of the abdominal organs, and smaller fetal kidney size with kidney function outcomes in school-aged children. We also explored whether any association was explained by childhood kidney size.     

Pseudouridine and uridine in normal kidney and kidney cancer tissues

Summary The tissue concentrations of a modified nucleoside, pseudouridine, and a normal nucleoside, uridine, were measured with high-performance liquid chromatography. Human kidneys were obtained from five patients with renal cell carcinoma and divided into a noncancerous part and a cancerous part. The pseudouridine concentration in the cancerous part of the kidneys ranged between<2–2.8 nmoles/g and in the noncancerous part 4.3–19.4 nmoles/g (mean 10,9 nmoles/g). The uridine concentration in the cancerous and noncancerous parts of the kidney ranged between 19.6–179.1 nmoles/g (mean 110.7 nmoles/g) and 117.5–235.6 nmoles/g (mean 191.5 nmoles/g), respectively. The pseudouridine concentration appeared to be approximately seven times higher in the noncancerous part as compared to the cancerous part of the kidney. In the case of uridine, the difference was less pronounced.     

Neural control of renal hemodynamics and function during development

This review summarizes our current understanding of the role of the renal sympathetic nervous system during development. Recent evidence suggests that renal innervation appears early during fetal life and may play an important role in promoting cellular development. It has also been observed that renal nerve stimulation decreases renal blood flow and increases renal vascular resistance in fetal sheep, but to a lesser extent than in newborn and adult sheep. Moreover, it has been shown that, contrary to previous findings in adult animals, renal nerve stimulation during -adrenoceptor blockade induces renal vasodilation in fetal and newborn sheep, but not in adult sheep. Recent studies have also demonstrated that renal nerves modulate the natriuretic response to a saline load in newborn lambs and influence sodium reabsorption in near-term fetal sheep. The role of renal nerves and neuronally released norepinephrine on renin secretion in the developing kidney is discussed. Finally, it is suggested that efferent renal sympathetic nerve activity might influence fetal renal hemodynamics during stressful conditions.     

Immediate and long-term renal effects of fetal exposure to gentamicin

Aminoglycoside antibiotics, like gentamicin, given to pregnant females cross the placenta and accumulate in the fetal kidney, which, like the adult kidney, was found to be the major site of deposition. In young guineapigs whose mothers were given gentamicin during the week following nephrogenesis in the fetus, nephron growth was found to be retarded temporarily. In rats whose mothers were given gentamicin during the period of fetal nephrogenesis, the final number of nephrons was reduced by about 20%. In both cases, renal development was imparied. although the concentration of gentamicin in the fetal kidney was lower than that measured in the kidney of human fetuses whose mothers had received a single injection of aminoglycoside. In rats exposed to gentamicin in utero, cellular damage of the undifferentiated and differentiating renal tissues was observed. It is, there are likely that the oligonephronia observed in animals born of gentamicin-treated mothers resulted from a direct effect of the drug at early stages of nephrogenesis. When gentamicin administration to the mother was prolonged, part of the oligonephronia observed at birth might have also resulted from fetal growth retardation, secondary to adverse effects of the drug on the mother. Providing it was not associated with fetal growth retardation, the presence of high gentamicin concentrations in the fetal kidney at late stages of nephrogenesis did not affect nephron differentiation. Long-term studies of rats born with gentamicin-induced oligone-phronia showed that neither the antibiotic still present in kidney several weeks after birth, nor the injuries it caused, prevented renal growth and morphological adaptation of the nephrons to their reduced number. This also holds true for functional adaptation, except in the case of phosphate transport. Of interest is the fact that the mild oligonephronia acquired in utero after exposure to gentamicin was sufficient to cause early development of glomerular sclerosis in the adults.     

Action of Estradiol on Epiphyseal Growth Plate Chondrocytes

Estrogen plays an important role in the human growth plate by accelerating growth and promoting epiphyseal fusion in both sexes. Nevertheless, the precise mechanisms responsible for these effects are poorly understood. In the present study, we examined the role of 17-estradiol (E2) on cell proliferation and viability, type X collagen synthesis, alkaline phosphatase activity, and matrix calcification in primary cultures of resting, proliferating, and prehypertrophic chondrocytes derived from explants of the bovine fetal epiphyseal growth plate. Growth plate chondrocytes were isolated and separated into maturationally distinct subpopulations, which were cultured for 7–21 days to high density in either (1) serum-free medium, (2) 1 nM thyroid hormone (T₃), (3) E2 concentrations ranging from 10^–13 M to 10^–7 M, or (4) a combination of T₃ and E2. To compare E2 effects in both sexes, chondrocytes were harvested from 8 fetuses of both sexes. After hormone treatment, cell cultures were analyzed for cell number and viability, collagen type X, alkaline phosphatase (ALP), and matrix calcification. Neither DNA content nor cell viability were affected by the duration or type of hormone treatment. By itself, E2 stimulated maturation of all subpopulations only in pharmacologic doses (10^–7 M). Physiologic E2 concentrations were no different than negative controls treated with ITS (insulin, transferrin, and selenite). Regardless of E2 concentrations, the addition of E2 to 1 nM T₃ did not appreciably affect the response to T₃ alone, which stimulates maturation of the phenotype. All effects were comparable in both male and female chondrocytes, in all cell subpopulations (maturation stages) and fetuses of varying gestational age. These findings indicate that at physiologic concentrations, the effects of E2 on fetal bovine growth plate chondrocyte appear to be indirect and independent of T₃, suggesting that, in vivo, E2 acts in concert with other factors or hormones to induce fusion of the growth plate.     

Is fetal tissue the only factor responsible for the properties of fetal wound healing?

Fetal skin wounds heal without inflammation, collagen deposition or wound contraction. The mechanism of this process is unknown, but may be unique to fetal cells, the fetal environment, or an combination of both. In order to determine whether fetal cells are the only factor responsible for scarless wound healing, an experimental study was performed on ten cats who were in the last trimester of their pregnancy. Skin grafts were transferred from mother to fetus and fetus to mother. The fetal skin grafted to the mother was biopsied between the eighth and tenth postoperative days and was evaluated histopathologically on days 18–20. Biopsy revealed scar formation in both the fetal grafts in the adult and maternal grafts in the fetus. We can conclude that scarless wound healing in the fetus is not solely due to fetal cells.     

Fetal MRI lung volumes are predictive of perinatal outcomes in fetuses with congenital lung masses

Purpose

The purpose of this study was to evaluate fetal magnetic resonance imaging (MRI) as a modality for predicting perinatal outcomes and lung-related morbidity in fetuses with congenital lung masses (CLM).

Methods

The records of all patients treated for CLM from 2002 to 2012 were reviewed retrospectively. Fetal MRI-derived lung mass volume ratio (LMVR), observed/expected normal fetal lung volume (O/E-NFLV), and lesion-to-lung volume ratio (LLV) were calculated. Multivariate regression and receiver operating characteristic analyses were applied to determine the predictive accuracy of prenatal imaging.

Results

Of 128 fetuses with CLM, 93% (n = 118) survived. MRI data were available for 113 fetuses. In early gestation (< 26 weeks), MRI measurements of LMVR and LLV correlated with risk of fetal hydrops, mortality, and/or need for fetal intervention. In later gestation (> 26 weeks), LMVR, LLV, and O/E-NFLV correlated with neonatal respiratory distress, intubation, NICU admission and need for neonatal surgery. On multivariate regression, LMVR was the strongest predictor for development of fetal hydrops (OR: 6.97, 1.58–30.84; p = 0.01) and neonatal respiratory distress (OR: 12.38, 3.52–43.61; p ≤ 0.001). An LMVR > 2.0 predicted worse perinatal outcome with 83% sensitivity and 99% specificity (AUC = 0.94; p < 0.001).

Conclusion

Fetal MRI volumetric measurements of lung masses and residual normal lung are predictive of perinatal outcomes in fetuses with CLM. These data may assist in perinatal risk stratification, counseling, and resource utilization.     

Prenatal diagnosis and management of bilateral hydronephrosis

This report reviews the management of the fetus with congenital hydronephrosis (CH), a challenging diagnostic and therapeutic problem. Experimental models of obstructive uropathy have produced histologic changes similar to those seen in kidneys of human neonates with congenital hydronephrosis. Relief of obstruction in utero in these models has been shown to prevent some of the dysplastic changes caused by obstruction. These studies have formed the theoretical basis for in utero decompression to restore amniotic fluid dynamics to prevent death from pulmonary hypoplasia, and reverse or arrest dysplastic morphogenesis. The development of prognostic criteria has greatly aided in selection of appropriate fetuses for intervention. These criteria include: (1) Na<100 mEq/l; (2) Cl<90 mEq/l; (3) osmolarity <210 mosmol; (4) sonographic appearance of the fetal kidneys; (5) amniotic fluid status; (6) urine output at fetal bladder catheterization. All fetuses should have ultrasonography to exclude other anomalies, and karyotype analysis to exclude chromosomal abnormality. If amniotic fluid volume is normal, the pregnancy is followed with serial ultrasound examinations. If oligohydramnios develops, a prognostic evaluation is performed, including fetal bladder catheterization. If the fetus has poor residual renal function, on the basis of prognostic criteria, appropriate counseling may be given. If the fetus has good residual renal function, depending on lung maturity, it can be delivered early for corrective surgery. If diagnosed prior to lung maturity in utero, decompression by either vesicoamniotic shunting or open fetal surgery may be attempted in the highly selected case. Very few fetuses with CH will require in utero decompression, but all benefit from early diagnosis allowing preparation for postnatal care. Open fetal surgery should be considered an experimental therapy until efficacy and safety are established in controlled trials.     

Is a vesicoamniotic shunt intrinsically bad? Shunting a normal fetal bladder

Introduction

We previously demonstrated that in utero vesicoamniotic shunting of obstructive uropathy in fetal lambs produces a shrunken noncompliant bladder. We hypothesized that the normal fetal bladder filling and emptying cycle in fetal life is critical to the development of normal bladder function.

Materials and Methods

We placed vesicoamniotic shunts in 4 normal fetal lambs at 74 days' gestation. The fetuses were delivered at term (145 days), and bladder volume and compliance were measured and compared with those measurements in 3 normal term fetuses. The lambs were then killed and the renal tracts and bladders removed submitted to histologic examination.

Results

All shunted lambs survived to term. Three normal control lambs were delivered at term. The mean bladder volume in shunted lambs was 4 ± 2.8 mL (n = 4) compared with 60 ± 17 mL (n = 3) in control lambs (P < .05). Bladders in the shunted lambs had very poor compliance compared with normal lambs' bladders. Histologic examination of the shunted bladders showed increased fibrosis and distortion of the muscle layers compared with control bladders.

Conclusion

Even in the absence of obstruction, preventing normal bladder filling and emptying in fetal life produces fibrotic bladders with poor compliance.