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Francoise Muller - One of the best experts on this subject based on the ideXlab platform.
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prenatal diagnosis of bartter syndrome Amniotic Fluid aldosterone
Annales De Biologie Clinique, 2017Co-Authors: Myriam Rachid, Rosa Vargaspoussou, Georges Deschênes, Sophie Dreux, Isabelle Czerkiewicz, Gauthier Pean De Ponfilly, D Chevenne, J F Oury, Francoise MullerAbstract:Bartter syndrome is a severe inherited tubulopathy characterized at birth by salt wasting, severe polyuria, dehydration, growth retardation and secondary hyperaldosteronism. Prenatally, the disease is usually discovered following onset of severe polyhydramnios. We studied Amniotic Fluid aldosterone concentration in cases of Bartter syndrome and in control groups. Amniotic Fluid aldosterone was assayed by radioimmunoassay. We undertook a retrospective case-control study based on 36 cases of postnatally diagnosed Bartter syndrome and 144 controls matched for gestational age. Two controls groups were defined: controls with polyhydramnios (n=72) and control without polyhydramnios (n=72). Amniotic Fluid aldosterone was compared between the three groups. The median Amniotic Fluid aldosterone concentration in the Bartter syndrome group (90 pg/mL) did not differ significantly from that in the controls with polyhydramnios (90 pg/mL, p=0.33) or the controls without polyhydramnios (87 pg/mL, p=0.41). In conclusion, Amniotic Fluid aldosterone assay cannot be used for prenatal diagnosis of Bartter syndrome.
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prenatal diagnosis of bartter syndrome Amniotic Fluid aldosterone
Prenatal Diagnosis, 2016Co-Authors: Myriam Rachid, Rosa Vargaspoussou, Georges Deschênes, Sophie Dreux, Isabelle Czerkiewicz, Gauthier Pean De Ponfilly, D Chevenne, J F Oury, Francoise MullerAbstract:Objective Bartter syndrome is a severe inherited tubulopathy characterized by postnatal salt wasting, severe polyuria, dehydration, failure to thrive and secondary hyperaldosteronism. Prenatally, the disease is usually discovered following the onset of severe polyhydramnios in the second trimester. We studied Amniotic Fluid aldosterone concentration in Bartter syndrome and in controls. Methods Amniotic Fluid aldosterone was assayed by radioimmunoassay. We undertook a retrospective case-control study based on 36 cases of prenatally suspected and postnatally confirmed Bartter syndrome (22 with identified mutations): and 72 gestational age matched controls presenting with polyhydramnios and 72 without polyhydramnios. Amniotic Fluid aldosterone was compared between the three groups. Results The median Amniotic Fluid aldosterone concentration in the Bartter syndrome group (90 pg/mL) was not different from that in the controls with polyhydramnios (90 pg/mL, P = 0.33) or without polyhydramnios (87 pg/mL, P = 0.41). Conclusion Amniotic Fluid aldosterone assay cannot be used for prenatal diagnosis of Bartter syndrome. © 2015 John Wiley & Sons, Ltd.
Roberto Romero - One of the best experts on this subject based on the ideXlab platform.
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lack of evidence for a viable microbiota in murine Amniotic Fluid
bioRxiv, 2021Co-Authors: Roberto Romero, Jose Galaz, Andrew D Winters, Jonathan M Greenberg, Zachary Shaffer, Valeria GarciafloresAbstract:The existence of an Amniotic Fluid microbiota (i.e., a viable microbial community) in mammals is controversial. Its existence would require a fundamental reconsideration of the role of intra-Amniotic microbes in fetal development and pregnancy outcomes. In this study, we determined whether the Amniotic Fluid of mice harbors a microbiota in late gestation. Bacterial profiles of Amniotic Fluids located proximally or distally to the cervix were characterized through quantitative real-time PCR, 16S rRNA gene sequencing, and culture (N = 21 mice). These profiles were compared to those of technical controls for background DNA contamination. The load of 16S rDNA in the Amniotic Fluid exceeded that in controls. Additionally, the 16S rDNA profiles of the Amniotic Fluid differed from those of controls, with Corynebacterium tuberculostearicum being differentially more abundant in Amniotic Fluid profiles; however, this bacterium was not cultured. Of the 42 total bacterial cultures of Amniotic Fluids, only one yielded bacterial growth - Lactobacillus murinus. The 16S rRNA gene of this common murine-associated bacterium was not detected in any Amniotic Fluid sample, suggesting it did not originate from the Amniotic Fluid. No differences in 16S rDNA load, 16S rDNA profile, or bacterial culture were observed between Amniotic Fluids located proximal and distal to the cervix. Collectively, these data show that, although there is a modest DNA signal of bacteria in murine Amniotic Fluid, there is no evidence that this signal represents a viable microbiota. These findings refute the proposed role of Amniotic Fluid as a source of microorganisms for in utero colonization. IMPORTANCEThe prevailing paradigm in obstetrics has been the sterile womb hypothesis, which posits that fetuses are first colonized by microorganisms during labor and/or the vaginal delivery process. However, it has been suggested that fetuses are consistently colonized in utero. One proposed source of colonizers is the Amniotic Fluid surrounding the fetus. This concept has been derived primarily from investigations that relied on DNA sequencing. Due to the low microbial biomass of Amniotic Fluid, such studies are susceptible to influences of background DNA contamination. Additionally, even if there is a microbial DNA signature in Amniotic Fluid, this is not necessarily reflective of a resident microbiota that could colonize the mammalian fetus. In the current study, using multiple microbiologic approaches and incorporating technical controls for DNA contamination, we show that, although there is a low abundance bacterial DNA signal in Amniotic Fluid, this does not translate to the presence of viable bacteria.
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cellular immune responses in Amniotic Fluid of women with a sonographic short cervix
Journal of Perinatal Medicine, 2020Co-Authors: Roberto Romero, Jose Galaz, Derek Miller, Dustyn Levenson, Robert ParaAbstract:Objectives A sonographic short cervix is one of the strongest predictors of preterm delivery. However, the cellular immune composition of Amniotic Fluid in women with a short cervix has not yet been described. Herein, we determined cellular and soluble immune responses in Amniotic Fluid from pregnant women with a mid-trimester asymptomatic short cervix. Methods Amniotic Fluid samples (n=77) were collected from asymptomatic women with a cervical length between 15 and 25 mm (n=36, short cervix) or ≤15 mm (n=41, severely short cervix) diagnosed by ultrasound. Flow cytometry and multiplex measurement of cytokines/chemokines were performed. Results (1) The cellular immune composition of Amniotic Fluid did not differ between women with a severely short cervix (≤15 mm) and those with a short cervix 15-25 mm; (2) Amniotic Fluid concentrations of multiple cytokines/chemokines were higher in women with a severely short cervix (≤15 mm) than in those with a short cervix 15-25 mm; (3) the cellular immune composition of Amniotic Fluid did not differ between women with a severely short cervix (≤15 mm) who ultimately underwent preterm delivery and those who delivered at term; and (4) Amniotic Fluid concentrations of IL-2, but not other immune mediators, were increased in women with a severely short cervix (≤15 mm) who ultimately delivered preterm compared to those who delivered at term. Conclusions Women with a severely short cervix (≤15 mm) have increased concentrations of pro-inflammatory mediators in the Amniotic cavity; yet, these do not translate to changes in the cellular immune response.
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cellular immune responses in Amniotic Fluid of women with preterm prelabor rupture of membranes
Journal of Perinatal Medicine, 2020Co-Authors: Roberto Romero, Jose Galaz, Rebecca Slutsky, Kenichiro Motomura, Robert Para, Percy PacoraAbstract:Background Preterm birth is the leading cause of perinatal morbidity and mortality. Preterm prelabor rupture of membranes (pPROM) occurs in 30% of preterm births; thus, this complication is a major contributor to maternal and neonatal morbidity. However, the cellular immune responses in Amniotic Fluid of women with pPROM have not been investigated. Methods Amniotic Fluid samples were obtained from women with pPROM and a positive (n = 7) or negative (n = 10) microbiological culture. Flow cytometry was performed to evaluate the phenotype and number of Amniotic Fluid leukocytes. The correlation between Amniotic Fluid immune cells and an interleukin-6 (IL-6) concentration or a white blood cell (WBC) count in Amniotic Fluid was calculated. Results Women with pPROM and a positive Amniotic Fluid culture had (1) a greater number of total leukocytes in Amniotic Fluid, including neutrophils and monocytes/macrophages and (2) an increased number of total T cells in Amniotic Fluid, namely CD4+ T cells and CD8+ T cells, but not B cells. The numbers of neutrophils and monocytes/macrophages were positively correlated with IL-6 concentrations and WBC counts in Amniotic Fluid of women with pPROM. Conclusion Women with pPROM and a positive Amniotic Fluid culture exhibit a more severe cellular immune response than those with a negative culture, which is associated with well-known markers of intra-Amniotic inflammation.
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cellular immune responses in Amniotic Fluid of women with preterm clinical chorioamnionitis
Inflammation Research, 2020Co-Authors: Roberto Romero, Jose Galaz, Derek Miller, Rebecca Slutsky, Dustyn Levenson, Chaurdong HsuAbstract:Preterm birth is the leading cause of neonatal morbidity and mortality worldwide. Some preterm births are associated with clinical chorioamnionitis; yet, this condition has been poorly investigated. Herein, we characterized the Amniotic Fluid cellular immune responses in women with preterm clinical chorioamnionitis. Amniotic Fluid samples were obtained from women with preterm clinical chorioamnionitis and a positive or negative microbiological culture (n = 17). The cellular composition of Amniotic Fluid was evaluated using fluorescence microscopy, scanning and transmission electron microscopy, and flow cytometry. Women without preterm clinical chorioamnionitis were also examined (n = 10). Amniotic Fluid from women with preterm clinical chorioamnionitis and a positive culture had: (1) abundant neutrophils associated with viable and non-viable bacteria, (2) neutrophils performing phagocytosis, (3) neutrophils forming NETs, (4) increased numbers of neutrophils, monocytes/macrophages, and CD4+ T cells, and (5) high expression of IL-1β by neutrophils and monocytes/macrophages. Amniotic Fluid from women with preterm clinical chorioamnionitis and proven infection tended to have fewer monocytes/macrophages and CD4+ T cells compared to those without chorioamnionitis. We provide the first morphologic and phenotypic characterization of the cellular immune responses in the Amniotic cavity of women with preterm clinical chorioamnionitis, a condition associated with adverse neonatal outcomes.
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the immunophenotype of Amniotic Fluid leukocytes in normal and complicated pregnancies
American Journal of Reproductive Immunology, 2018Co-Authors: Roberto Romero, Derek Miller, Nardhy Gomezlopez, Yaozhu Leng, Bogdan Panaitescu, Pablo SilvaAbstract:PROBLEM The immune cellular composition of Amniotic Fluid is poorly understood. Herein, we determined: 1) the immunophenotype of Amniotic Fluid immune cells during the second and third trimester in the absence of intra-Amniotic infection/inflammation; 2) whether Amniotic Fluid T cells and ILCs display different phenotypical characteristics to that of peripheral cells; and 3) whether the Amniotic Fluid immune cells are altered in women with intra-Amniotic infection/inflammation. METHOD OF STUDY Amniotic Fluid samples (n = 57) were collected from 15 to 40 weeks of gestation in women without intra-Amniotic infection/inflammation. Samples from women with intra-Amniotic infection/inflammation were also included (n = 9). Peripheral blood mononuclear cells from healthy adults were used as controls (n = 3). Immunophenotyping was performed using flow cytometry. RESULTS In the absence of intra-Amniotic infection/inflammation, the Amniotic Fluid contained several immune cell populations between 15 and 40 weeks. Among these immune cells: (i) T cells and ILCs were greater than B cells and natural killer (NK) cells between 15 and 30 weeks; (ii) T cells were most abundant between 15 and 30 weeks; (iii) ILCs were most abundant between 15 and 20 weeks; (iv) B cells were scarce between 15 and 20 weeks; yet, they increased and were constant after 20 weeks; (v) NK cells were greater between 15 and 30 weeks than at term; (vi) ILCs expressed high levels of RORγt, CD161, and CD103 (ie, group 3 ILCs); (vii) T cells expressed high levels of RORγt; (viii) neutrophils increased as gestation progressed; and (ix) monocytes/macrophages emerged after 20 weeks and remained constant until term. All of the Amniotic Fluid immune cells, except ILCs, were increased in the presence of intra-Amniotic infection/inflammation. CONCLUSION The Amniotic Fluid harbors a diverse immune cellular composition during normal and complicated pregnancies.
R E De Filippo - One of the best experts on this subject based on the ideXlab platform.
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injection of Amniotic Fluid stem cells delays progression of renal fibrosis
Journal of The American Society of Nephrology, 2012Co-Authors: Sargis Sedrakya, R E De Filippo, Stefano Da Sacco, Anna Milanesi, Liro Shiri, Astgik Petrosya, Radka Varimezova, David Warburto, Kevi V Lemley, Laura PeriAbstract:Injection of Amniotic Fluid stem cells ameliorates the acute phase of acute tubular necrosis in animals by promoting proliferation of injured tubular cells and decreasing apoptosis, but whether these stem cells could be of benefit in CKD is unknown. Here, we used a mouse model of Alport syndrome, Col4a5−/− mice, to determine whether Amniotic Fluid stem cells could modify the course of progressive renal fibrosis. Intracardiac administration of Amniotic Fluid stem cells before the onset of proteinuria delayed interstitial fibrosis and progression of glomerular sclerosis, prolonged animal survival, and ameliorated the decline in kidney function. Treated animals exhibited decreased recruitment and activation of M1-type macrophages and a higher proportion of M2-type macrophages, which promote tissue remodeling. Amniotic Fluid stem cells did not differentiate into podocyte-like cells and did not stimulate production of the collagen IVa5 needed for normal formation and function of the glomerular basement membrane. Instead, the mechanism of renal protection was probably the paracrine/endocrine modulation of both profibrotic cytokine expression and recruitment of macrophages to the interstitial space. Furthermore, injected mice retained a normal number of podocytes and had better integrity of the glomerular basement membrane compared with untreated Col4a5−/− mice. Inhibition of the renin-angiotensin system by Amniotic Fluid stem cells may contribute to these beneficial effects. In conclusion, treatment with Amniotic Fluid stem cells may be beneficial in kidney diseases characterized by progressive renal fibrosis.
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renal differentiation of Amniotic Fluid stem cells
Cell Proliferation, 2007Co-Authors: Laura Perin, Stefano Giuliani, Daniel H Jin, Sargis Sedrakyan, Gianni Carraro, R Habibian, David Warburton, Anthony Atala, R E De FilippoAbstract:Objectives : The role of stem cells in regenerative medicine is evolving rapidly. Here, we describe the application, for kidney regeneration, of a novel non-genetically modified stem cell, derived from human Amniotic Fluid. We show that these pluripotent cells can develop and differentiate into de novo kidney structures during organogenesis in vitro . Materials and methods : Human Amniotic Fluid-derived stem cells (hAFSCs) were isolated from human male Amniotic Fluid obtained between 12 and 18 weeks gestation. Green fluorescent protein and Lac-Z-transfected hAFSCs were microinjected into murine embryonic kidneys (12.5-18 days gestation) and were maintained in a special co-culture system in vitro for 10 days. Techniques of live microscopy, histology, chromogenic in situ hybridization and reverse transcriptase polymerase chain reaction were used to characterize the hAFSCs during their integration and differentiation in concert with the growing organ. Results : Green fluorescent protein and Lac-Z- transfected hAFSCs demonstrated long-term viability in organ culture. Histological analysis of injected kidneys revealed that hAFSCs were capable of contributing to the development of primordial kidney structures including renal vesicle, C- and S-shaped bodies. Reverse transcriptase polymerase chain reaction confirmed expression of early kidney markers for: zona occludens-1, glial-derived neurotrophic factor and claudin. Conclusions : Human Amniotic Fluid-derived stem cells may represent a potentially limitless source of ethically neutral, unmodified pluripotential cells for kidney regeneration.
Steven L Clark - One of the best experts on this subject based on the ideXlab platform.
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proposed diagnostic criteria for the case definition of Amniotic Fluid embolism in research studies
American Journal of Obstetrics and Gynecology, 2016Co-Authors: Steven L Clark, Roberto Romero, Gary D V Hankins, Gary A Dildy, William M Callaghan, Richard Smiley, Arthur W Bracey, Mary E Dalton, Mike Foley, Luis D PachecoAbstract:Amniotic Fluid embolism is a leading cause of maternal mortality in developed countries. Our understanding of risk factors, diagnosis, treatment, and prognosis is hampered by a lack of uniform clinical case definition; neither histologic nor laboratory findings have been identified unique to this condition. Amniotic Fluid embolism is often overdiagnosed in critically ill peripartum women, particularly when an element of coagulopathy is involved. Previously proposed case definitions for Amniotic Fluid embolism are nonspecific, and when viewed through the eyes of individuals with experience in critical care obstetrics, would include women with a number of medical conditions much more common than Amniotic Fluid embolism. We convened a working group under the auspices of a committee of the Society for Maternal-Fetal Medicine and the Amniotic Fluid Embolism Foundation whose task was to develop uniform diagnostic criteria for the research reporting of Amniotic Fluid embolism. These criteria rely on the presence of the classic triad of hemodynamic and respiratory compromise accompanied by strictly defined disseminated intravascular coagulopathy. It is anticipated that limiting research reports involving Amniotic Fluid embolism to women who meet these criteria will enhance the validity of published data and assist in the identification of risk factors, effective treatments, and possibly useful biomarkers for this condition. A registry has been established in conjunction with the Perinatal Research Branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development to collect both clinical information and laboratory specimens of women with suspected Amniotic Fluid embolism in the hopes of identifying unique biomarkers of this condition.
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Amniotic Fluid embolism diagnosis and management
American Journal of Obstetrics and Gynecology, 2016Co-Authors: Luis D Pacheco, George R Saade, Gary D V Hankins, Steven L ClarkAbstract:Objective We sought to provide evidence-based guidelines regarding the diagnosis and management of Amniotic Fluid embolism. Study Design A systematic literature review was performed using MEDLINE, PubMed, EMBASE, and the Cochrane Library. The search was restricted to English-language articles published from 1966 through March 2015. Priority was given to articles reporting original research, in particular randomized controlled trials, although review articles and commentaries were consulted. Abstracts of research presented at symposia and scientific conferences were not considered adequate for inclusion. Evidence reports and published guidelines were also reviewed, and additional studies were located by reviewing bibliographies of identified articles. Grading of Recommendations Assessment, Development, and Evaluation (GRADE) methodology was used for defining the strength of recommendations and rating quality of the evidence. Consistent with US Preventive Task Force guidelines, references were evaluated for quality based on the highest level of evidence. Results and Recommendations We recommend the following: (1) we recommend consideration of Amniotic Fluid embolism in the differential diagnosis of sudden cardiorespiratory collapse in the laboring or recently delivered woman (GRADE 1C); (2) we do not recommend the use of any specific diagnostic laboratory test to either confirm or refute the diagnosis of Amniotic Fluid embolism; at the present time, Amniotic Fluid embolism remains a clinical diagnosis (GRADE 1C); (3) we recommend the provision of immediate high-quality cardiopulmonary resuscitation with standard basic cardiac life support and advanced cardiac life support protocols in patients who develop cardiac arrest associated with Amniotic Fluid embolism (GRADE 1C); (4) we recommend that a multidisciplinary team including anesthesia, respiratory therapy, critical care, and maternal-fetal medicine should be involved in the ongoing care of women with AFE (Best Practice); (5) following cardiac arrest with Amniotic Fluid embolism, we recommend immediate delivery in the presence of a fetus ≥23 weeks of gestation (GRADE 2C); (6) we recommend the provision of adequate oxygenation and ventilation and, when indicated by hemodynamic status, the use of vasopressors and inotropic agents in the initial management of Amniotic Fluid embolism. Excessive Fluid administration should be avoided (GRADE 1C); and (7) because coagulopathy may follow cardiovascular collapse with Amniotic Fluid embolism, we recommend the early assessment of clotting status and early aggressive management of clinical bleeding with standard massive transfusion protocols (GRADE 1C).
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Amniotic Fluid embolism analysis of the national registry
American Journal of Obstetrics and Gynecology, 1995Co-Authors: Gary D V Hankins, Steven L Clark, Donald A Dudley, Gary A Dildy, Flint T PorterAbstract:Abstract OBJECTIVE: We analyzed the clinical course and investigated possible pathophysiologic mechanisms Amniotic Fluid embolism. STUDY DESIGN: We carried out a retrospective review of medical records. Forty-six charts were analyzed for 121 separate clinical variables. RESULTS: Amniotic Fluid embolism occurred during labor in 70% of the women, after vaginal delivery in 11%, and during cesarean section after delivery of the infant in 19%. No correlation was seen with prolonged labor or oxytocin use. A significant relation was seen between Amniotic Fluid embolism and male fetal sex. Forty-one percent of patients gave a history of allergy or atopy. Maternal mortality was 61%, with neurologically intact survival seen in 15% of women. Of fetuses in utero at the time of the ovent, only 39% survived. Clinical and hemodynamic manifestations were similar to those manifest in anaphytaxis and septic shock. CONCLUSIONS: Intact maternal or fetal survival with Amniotic Fluid embolism is rare. The striking similarities between clinical and hemodynamic findings in Amniotic Fluid embolism and both anaphylaxis and septic shock suggest a common pathophysiologic mechanism for all these conditions. Thus the term Amniotic Fluid embolism appears to be a misnomer.
Myriam Rachid - One of the best experts on this subject based on the ideXlab platform.
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prenatal diagnosis of bartter syndrome Amniotic Fluid aldosterone
Annales De Biologie Clinique, 2017Co-Authors: Myriam Rachid, Rosa Vargaspoussou, Georges Deschênes, Sophie Dreux, Isabelle Czerkiewicz, Gauthier Pean De Ponfilly, D Chevenne, J F Oury, Francoise MullerAbstract:Bartter syndrome is a severe inherited tubulopathy characterized at birth by salt wasting, severe polyuria, dehydration, growth retardation and secondary hyperaldosteronism. Prenatally, the disease is usually discovered following onset of severe polyhydramnios. We studied Amniotic Fluid aldosterone concentration in cases of Bartter syndrome and in control groups. Amniotic Fluid aldosterone was assayed by radioimmunoassay. We undertook a retrospective case-control study based on 36 cases of postnatally diagnosed Bartter syndrome and 144 controls matched for gestational age. Two controls groups were defined: controls with polyhydramnios (n=72) and control without polyhydramnios (n=72). Amniotic Fluid aldosterone was compared between the three groups. The median Amniotic Fluid aldosterone concentration in the Bartter syndrome group (90 pg/mL) did not differ significantly from that in the controls with polyhydramnios (90 pg/mL, p=0.33) or the controls without polyhydramnios (87 pg/mL, p=0.41). In conclusion, Amniotic Fluid aldosterone assay cannot be used for prenatal diagnosis of Bartter syndrome.
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prenatal diagnosis of bartter syndrome Amniotic Fluid aldosterone
Prenatal Diagnosis, 2016Co-Authors: Myriam Rachid, Rosa Vargaspoussou, Georges Deschênes, Sophie Dreux, Isabelle Czerkiewicz, Gauthier Pean De Ponfilly, D Chevenne, J F Oury, Francoise MullerAbstract:Objective Bartter syndrome is a severe inherited tubulopathy characterized by postnatal salt wasting, severe polyuria, dehydration, failure to thrive and secondary hyperaldosteronism. Prenatally, the disease is usually discovered following the onset of severe polyhydramnios in the second trimester. We studied Amniotic Fluid aldosterone concentration in Bartter syndrome and in controls. Methods Amniotic Fluid aldosterone was assayed by radioimmunoassay. We undertook a retrospective case-control study based on 36 cases of prenatally suspected and postnatally confirmed Bartter syndrome (22 with identified mutations): and 72 gestational age matched controls presenting with polyhydramnios and 72 without polyhydramnios. Amniotic Fluid aldosterone was compared between the three groups. Results The median Amniotic Fluid aldosterone concentration in the Bartter syndrome group (90 pg/mL) was not different from that in the controls with polyhydramnios (90 pg/mL, P = 0.33) or without polyhydramnios (87 pg/mL, P = 0.41). Conclusion Amniotic Fluid aldosterone assay cannot be used for prenatal diagnosis of Bartter syndrome. © 2015 John Wiley & Sons, Ltd.