Cases reported "Oligohydramnios"

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1/35. prenatal diagnosis of nonmosaic trisomy 9 in a fetus with severe renal disease.

    We report a case of nonmosaic trisomy 9 presenting at 21 weeks of gestation with polycystic, echogenic horseshoe kidney, collapsed bladder, absent amniotic fluid, and intrauterine growth restriction. color Doppler imaging demonstrated no blood flow signals from renal vessels. fetal blood sampling confirmed a 47,XX, 9 karyotype, with no evidence of mosaicism, and increased serum beta2-microglobulin levels of 10.7 mg/l, consistent with severe renal failure. A repeat scan at 23 weeks also revealed a dysmorphic face, bilateral microphthalmia, and a cerebellar vermian defect. Follow-up examinations showed progressive growth restriction leading to fetal death at 33 weeks of gestation. This report demonstrates that fetuses with nonmosaic trisomy 9 may present with severe renal abnormalities and confirms that cases seen in the second and third trimesters usually have a dismal outcome.
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2/35. Bilateral renal agenesis and fetal ascites in association with partial trisomy 13 and partial trisomy 16 due to a 3:1 segregation of maternal reciprocal translocation t(13;16)(q12.3; p13.2).

    A female fetus with bilateral renal agenesis and fetal ascites was found to have partial trisomy 13 (pter-q12.3) and partial trisomy 16 (p13.2-pter), 47,XX, der(13)t(13;16)(q12.3; p13.2)mat. The chromosomal aberration was due to a 3:1 segregation with tertiary trisomy transmitted from a maternal reciprocal translocation 13;16. Prenatal ultrasound of a 29-year-old, gravida 2, para 0 woman at 22 gestational weeks showed fetal ascites, severe oligohydramnios and non-visualization of fetal urinary bladder and kidneys. The pregnancy was terminated. At delivery, the proband displayed dysmorphic features of hypertelorism, a prominent glabella, epicanthic fold, a stubby nose with a depressed nasal bridge, anteverted nares, thin lips, micrognathia, low-set ears, a short neck and a distended abdomen. Necropsy confirmed bilateral renal agenesis and ascites. A cytogenetic study performed on fibroblasts obtained from the proband's skin revealed an extra supernumerary chromosome. The mother was later found to have a reciprocal translocation. fluorescence in situ hybridization for a submicroscopic deletion in chromosome 22q11 in the proband was negative. The parents had no urological anomalies. Our observation further extends the clinical spectrum associated with proximal trisomy 13q and distal trisomy 16p. We suggest prenatal cytogenetic analysis in fetuses with urological anomalies, including renal agenesis, to uncover underlying genetic disorders.
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3/35. Prenatally diagnosed autosomal recessive polycystic kidney disease: initial postnatal management.

    We report a case of autosomal recessive polycystic kidney disease (ARPKD). A presumptive diagnosis was made after a late-term prenatal ultrasound revealed hypoplastic lungs, massive polycystic kidneys, and oligohydramnios. A full-term baby girl was delivered vaginally. Respiratory distress required intubation. Twelve hours after birth, she underwent bilateral nephrectomy and peritoneal dialysis catheter placement. The average kidney size was 150 g and 9.25 cm. Pathologic examination confirmed ARPKD. peritoneal dialysis was started on the third day of life. The baby had no gross neurologic deficit. At 6 months of age, she was growing well, and the mother was a candidate to be a living-related kidney donor.
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4/35. Severe oligohydramnios induced by cyclooxygenase-2 inhibitor nimesulide.

    BACKGROUND: Cyclooxygenase-2 inhibitors might have fewer adverse fetal effects than conventional nonsteroidal anti-inflammatory drugs that inhibit both isoforms of the enzyme. Although cyclooxygenase-2 is expressed in fetal kidneys, there are no reports of adverse effects in human pregnancy. CASE: A 27-year-old woman, gravida 2, para 0, with a twin pregnancy at 24 weeks' gestation had placement of a cervical cerclage. Nimesulide was prescribed for postoperative preterm labor prophylaxis. Three weeks later, severe oligohydramnios was identified in both sacs, despite normal growth, renal anatomy, and umbilical artery and renal artery Doppler flow velocimetry. After stopping the drug, amniotic fluid volumes returned to normal over 2 weeks. There were no adverse neonatal renal effects. CONCLUSION: Selective cyclooxygenase-2 inhibition might cause severe oligohydramnios. If it is used, we advise close fetal surveillance.
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5/35. Renal tubular dysgenesis (RTD) - an important cause of the oligohydramnion-sequence. Report of 3 cases and review of the literature.

    Renal tubular dysgenesis (RTD) is a disorder characterized by neonatal renal failure and regular gross renal architecture, although the histological features of immature and shortened proximal tubules lead to neonatal death. The pathogenesis of this condition includes a congenital familial condition, a twin-twin transfusion syndrome, and an angiotensin-converting enzyme inhibitor intake by the mother. The clinical picture shows an association with oligohydramnia, pulmonary hypoplasia, and skull ossification defects. In the present paper, we report the occurrence of RTD in three infants of a consanguinous couple and compared our data with those of the literature. Our data confirm that late second trimester demonstration of oligohydramnion, with structurally normal kidneys and with or without skull ossification defects, allows the diagnosis of renal tubular dysgenesis, which, however, has to be confirmed by histological and immunohistological examinations of the kidney.
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6/35. First-trimester diagnosis of sirenomelia. A case report.

    We report a case of sirenomelia diagnosed at 13 gestational weeks. This rare malformation sequence is characterized by fusion and rotation of the lower limbs to various degrees and anorectal atresia, usually associated with absence of bladder and agenesis or dysgenesis of the kidneys. Diagnosis is commonly made later in the second trimester of pregnancy with oligohydramnios as the alerting sign. survival is extremely rare, and only possible in the absence of bilateral renal agenesis. In view of the dismal prognosis, early diagnosis allows for earlier and less traumatic therapeutic abortion.
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7/35. Meckel Gruber syndrome--a single gene cause of recurrent neural tube defects.

    Meckel Gruber syndrome (MGS), an autosomal recessive disorder characterised by posterior encephalocoele, multicystic kidneys and post-axial polydactyly should be recognised by obstetricians and paediatricians to counsel parents regarding the 25% recurrence risk. We report a consanguineous family with MGS affecting three infants.
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8/35. prenatal diagnosis of multiple acyl-coa dehydrogenase deficiency: association with elevated alpha-fetoprotein and cystic renal changes.

    We report the occurrence of multiple acyl-coa dehydrogenase deficiency (MADD) in two consecutive pregnancies in a young, Caucasian, non-consanguineous couple. In the first pregnancy, the maternal serum alpha-fetoprotein was elevated. A sonogram showed growth delay, cystic renal disease, and oligohydramnios; the parents decided to terminate the pregnancy. Postmortem examination confirmed the cystic renal disease and showed hepatic steatosis, raising the suspicion of a metabolic disorder. The diagnosis of MADD was made by immunoblot studies on cultured fibroblasts. In the subsequent pregnancy, a sonogram at 15 weeks' gestation showed an early growth delay but normal kidneys. The maternal serum and amniotic fluid concentrations of alpha-fetoprotein were elevated, and the amniotic fluid acylcarnitine profile was consistent with MADD. in vitro metabolic studies on cultured amniocytes confirmed the diagnosis. A follow-up sonogram showed cystic renal changes. These cases provide additional information regarding the evolution of renal changes in affected fetuses and show a relationship with elevated alpha-fetoprotein, which may be useful in counseling the couple at risk. MADD should be considered in the differential diagnosis of elevated alpha-fetoprotein and cystic renal disease. Early growth delay may be an additional feature.
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9/35. Penile agenesis complicated by Potter sequence.

    We present a case of penile agenesis complicated by multicystic dysplastic kidneys and urethral agenesis, which resulted in oligohydramnios, pulmonary hypoplasia and neonatal death. In this case, no external urethral opening was found, and the gastrointestinal tract showed no anomaly. Cases of penile agenesis complicated by Potter sequence with urethral agenesis should be differentiated from those with ectopic urethral openning.
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10/35. Renal tubular dysgenesis and neonatal hemochromatosis without pulmonary hypoplasia.

    Renal tubular dysgenesis is a rare disorder of differentiation of the fetal kidney. The condition has previously been reported as a postmortem diagnosis in infants who have had oligohydramnios commencing after 20 weeks gestation and have died of renal or respiratory failure shortly after birth with a clinical description of Potter sequence. The absence of clinically significant pulmonary hypoplasia in our case serves to emphasize that renal tubular dysgenesis, fetal anuria and long-standing oligohydramnios can occur without pulmonary insufficiency. The coexistence of renal tubular dysgenesis with neonatal hemochromatosis has been previously described in four published cases. The link between these two rare conditions is clinically important if dialysis or liver transplantation is considered in infants with hepatic and renal failure. Antemortem diagnosis by renal biopsy in our case enabled parental counseling and avoided the inappropriate use of peritoneal dialysis.
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