Standard

Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios? / van Gemert, Martin J. C.; Nikkels, Peter G. J.; Ross, Michael G.; van den Wijngaard, Jeroen P. H. M.

In: Birth defects research, Vol. 113, No. 6, 01.04.2021, p. 500-510.

Research output: Contribution to journalArticleAcademicpeer-review

Harvard

van Gemert, MJC, Nikkels, PGJ, Ross, MG & van den Wijngaard, JPHM 2021, 'Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?', Birth defects research, vol. 113, no. 6, pp. 500-510. https://doi.org/10.1002/bdr2.1874

APA

van Gemert, M. J. C., Nikkels, P. G. J., Ross, M. G., & van den Wijngaard, J. P. H. M. (2021). Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios? Birth defects research, 113(6), 500-510. https://doi.org/10.1002/bdr2.1874

Vancouver

van Gemert MJC, Nikkels PGJ, Ross MG, van den Wijngaard JPHM. Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios? Birth defects research. 2021 Apr 1;113(6):500-510. https://doi.org/10.1002/bdr2.1874

Author

van Gemert, Martin J. C. ; Nikkels, Peter G. J. ; Ross, Michael G. ; van den Wijngaard, Jeroen P. H. M. / Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?. In: Birth defects research. 2021 ; Vol. 113, No. 6. pp. 500-510.

BibTeX

@article{83a6f180aad14374b18a4bb59b6dc3b9,
title = "Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?",
abstract = "Background: Acardiac twinning is a complication of monochorionic twin pregnancies. From literature reports, 30 of 41 relatively large acardiac twins with renal tissue produced polyhydramnios within their amniotic compartment. We aim to investigate the underlying mechanisms that cause excess amniotic fluid using an established model of fetal fluid dynamics. Methods: We assumed that acardiac onset is before 13 weeks, acardiacs with renal tissue have normal kidney function and produce urine flow from 11 weeks on, and acardiac urine production requires a pressure of half the pump twin's mean arterial pressure. We apply a resistance network with the pump twin's arterio-venous pressure as source, pump umbilical arteries, placenta, placental arterio-arterial (AA) anastomoses and acardiac resistances. Acardiac amniotic fluid dynamics excluded acardiac lung fluid secretion, swallowing and the relatively small intramembranous flow. Results: In small acardiacs with sufficient urine production, polyhydramnios will occur due to the lack of amniotic fluid resorption. Urine production is dependent upon having sufficient mean arterial pressure, which requires nearly a two-fold larger resistance within the acardiac as compared to the placental AA resistance. Subphysiologic arterial pressure may result in renal dysgenesis. Conclusion: Our findings suggest the potential for prediction of which clinical acardiac cases may or may not develop polyhydramnios based upon noninvasive assessments of renal tissue, blood flow and urine production. This information would be of great value in determining early obstetric interventions as opposed to conservative management. These findings may also contribute to an improved knowledge of the fascinating pathophysiology that surrounds acardiac twinning.",
keywords = "acardiac onset, acardiac twin with renal tissue, acardiac twinning, amniotic fluid dynamics, arterio-arterial anastomosis, computational model simulations, fetoplacental resistance network, intramembranous flow, polyhydramnios, urine production",
author = "{van Gemert}, {Martin J. C.} and Nikkels, {Peter G. J.} and Ross, {Michael G.} and {van den Wijngaard}, {Jeroen P. H. M.}",
note = "Publisher Copyright: {\textcopyright} 2021 The Authors. Birth Defects Research published by Wiley Periodicals LLC. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.",
year = "2021",
month = apr,
day = "1",
doi = "10.1002/bdr2.1874",
language = "English",
volume = "113",
pages = "500--510",
journal = "Birth defects research",
issn = "2472-1727",
publisher = "John Wiley and Sons Ltd",
number = "6",

}

RIS

TY - JOUR

T1 - Acardiac twin pregnancies part V: Why does an acardiac twin with renal tissue produce polyhydramnios?

AU - van Gemert, Martin J. C.

AU - Nikkels, Peter G. J.

AU - Ross, Michael G.

AU - van den Wijngaard, Jeroen P. H. M.

N1 - Publisher Copyright: © 2021 The Authors. Birth Defects Research published by Wiley Periodicals LLC. Copyright: Copyright 2021 Elsevier B.V., All rights reserved.

PY - 2021/4/1

Y1 - 2021/4/1

N2 - Background: Acardiac twinning is a complication of monochorionic twin pregnancies. From literature reports, 30 of 41 relatively large acardiac twins with renal tissue produced polyhydramnios within their amniotic compartment. We aim to investigate the underlying mechanisms that cause excess amniotic fluid using an established model of fetal fluid dynamics. Methods: We assumed that acardiac onset is before 13 weeks, acardiacs with renal tissue have normal kidney function and produce urine flow from 11 weeks on, and acardiac urine production requires a pressure of half the pump twin's mean arterial pressure. We apply a resistance network with the pump twin's arterio-venous pressure as source, pump umbilical arteries, placenta, placental arterio-arterial (AA) anastomoses and acardiac resistances. Acardiac amniotic fluid dynamics excluded acardiac lung fluid secretion, swallowing and the relatively small intramembranous flow. Results: In small acardiacs with sufficient urine production, polyhydramnios will occur due to the lack of amniotic fluid resorption. Urine production is dependent upon having sufficient mean arterial pressure, which requires nearly a two-fold larger resistance within the acardiac as compared to the placental AA resistance. Subphysiologic arterial pressure may result in renal dysgenesis. Conclusion: Our findings suggest the potential for prediction of which clinical acardiac cases may or may not develop polyhydramnios based upon noninvasive assessments of renal tissue, blood flow and urine production. This information would be of great value in determining early obstetric interventions as opposed to conservative management. These findings may also contribute to an improved knowledge of the fascinating pathophysiology that surrounds acardiac twinning.

AB - Background: Acardiac twinning is a complication of monochorionic twin pregnancies. From literature reports, 30 of 41 relatively large acardiac twins with renal tissue produced polyhydramnios within their amniotic compartment. We aim to investigate the underlying mechanisms that cause excess amniotic fluid using an established model of fetal fluid dynamics. Methods: We assumed that acardiac onset is before 13 weeks, acardiacs with renal tissue have normal kidney function and produce urine flow from 11 weeks on, and acardiac urine production requires a pressure of half the pump twin's mean arterial pressure. We apply a resistance network with the pump twin's arterio-venous pressure as source, pump umbilical arteries, placenta, placental arterio-arterial (AA) anastomoses and acardiac resistances. Acardiac amniotic fluid dynamics excluded acardiac lung fluid secretion, swallowing and the relatively small intramembranous flow. Results: In small acardiacs with sufficient urine production, polyhydramnios will occur due to the lack of amniotic fluid resorption. Urine production is dependent upon having sufficient mean arterial pressure, which requires nearly a two-fold larger resistance within the acardiac as compared to the placental AA resistance. Subphysiologic arterial pressure may result in renal dysgenesis. Conclusion: Our findings suggest the potential for prediction of which clinical acardiac cases may or may not develop polyhydramnios based upon noninvasive assessments of renal tissue, blood flow and urine production. This information would be of great value in determining early obstetric interventions as opposed to conservative management. These findings may also contribute to an improved knowledge of the fascinating pathophysiology that surrounds acardiac twinning.

KW - acardiac onset

KW - acardiac twin with renal tissue

KW - acardiac twinning

KW - amniotic fluid dynamics

KW - arterio-arterial anastomosis

KW - computational model simulations

KW - fetoplacental resistance network

KW - intramembranous flow

KW - polyhydramnios

KW - urine production

UR - http://www.scopus.com/inward/record.url?scp=85100164961&partnerID=8YFLogxK

U2 - 10.1002/bdr2.1874

DO - 10.1002/bdr2.1874

M3 - Article

C2 - 33529493

VL - 113

SP - 500

EP - 510

JO - Birth defects research

JF - Birth defects research

SN - 2472-1727

IS - 6

ER -

ID: 15599630