The placenta contributes to activation of the renin angiotensin system in twin-twin transfusion syndrome

Galea, P., Barigye, O., Wee, L., Jain, V., Sullivan, M. and Fisk, N. M. (2008) The placenta contributes to activation of the renin angiotensin system in twin-twin transfusion syndrome. Placenta, 29 8: 734-742. doi:10.1016/j.placenta.2008.04.010


Author Galea, P.
Barigye, O.
Wee, L.
Jain, V.
Sullivan, M.
Fisk, N. M.
Title The placenta contributes to activation of the renin angiotensin system in twin-twin transfusion syndrome
Journal name Placenta   Check publisher's open access policy
ISSN 1532-3102
1532-3102
0265-7023
Publication date 2008-08-01
Year available 2008
Sub-type Article (original research)
DOI 10.1016/j.placenta.2008.04.010
Open Access Status
Volume 29
Issue 8
Start page 734
End page 742
Total pages 9
Editor Gernot Desoye
D. M. Nelson
Place of publication London, U.K.
Publisher W.B. Saunders
Language eng
Subject C1
111402 Obstetrics and Gynaecology
920114 Reproductive System and Disorders
1114 Paediatrics and Reproductive Medicine
Abstract The renin-angiotensin system (RAS) in twin-twin transfusion syndrome (TTTS) is Up-regulated in the donor Fetus's kidneys.. but down-regulated in the recipient's. Ultrasonographic and echocardiographic features suggest that the recipient is also exposed to RAS components. fit this stuck, we investigated the role and origin of RAS components in the recipient fetus. Monochorionic diamniotic (MCDA) pregnancies were recruited from a tertiary fetal medicine service. Cord blood was collected from MCDA twins (TTTS and control non-TTTS) at delivery for renin and angiotensin II immunoassays. Placental tissue was flash-frozen for mRNA and protein expression or formalin-fixed For immunohistochemistry. Archival placenta and kidney samples Were used for immunohistochemistry and in-situ hybridization. Plasma renin levels were elevated (p < 0.05) in recipients (median 201 pg/ml, range 54-315 pg/ml) and donors (125 pg/ml 25-296) with TTTS compared to controls (22.5 pg/ml, 1.1-1.5 The same was found with angiotensin II with high levels in both recipients (300.5 pg/ml, 86.1-488 pg/ml) and donors (239 p-/ml 76.6-422) compared to controls (169.5 pg/ml 89-220 pg/ml, p < 0.05). Renin mRNA expression, and protein appeared qualitatively higher ill the placental territory of the recipient compared to that of the donor and non-TTTS controls. We conclude that both fetuses in TTTS are exposed to high levels of RAS components: these appear to be produced from different sites, namely the kidney of the donor, and the placenta of the recipient. Given the markedly different phenotypes in the genetically identical fetuses with TTTS. we suo est that the Source of RAS components may influence their clinical manifestations. (C) 2008 Elsevier Ltd. All rights reserved.
Formatted abstract
The renin-angiotensin system (RAS) in twin–twin transfusion syndrome (TTTS) is up-regulated in the donor fetus's kidneys, but down-regulated in the recipient's. Ultrasonographic and echocardiographic features suggest that the recipient is also exposed to RAS components. In this study we investigated the role and origin of RAS components in the recipient fetus. Monochorionic diamniotic (MCDA) pregnancies were recruited from a tertiary fetal medicine service. Cord blood was collected from MCDA twins (TTTS and control non-TTTS) at delivery for renin and angiotensin II immunoassays. Placental tissue was flash-frozen for mRNA and protein expression or formalin-fixed for immunohistochemistry. Archival placenta and kidney samples were used for immunohistochemistry and in-situ hybridization. Plasma renin levels were elevated (p<0.05) in recipients (median 201pg/ml, range 54–315pg/ml) and donors (125pg/ml, 25–296) with TTTS compared to controls (2.5pg/ml, 1.1–1.5pg/ml). The same was found with angiotensin II with high levels in both recipients (300.5pg/ml, 86.1–488pg/ml) and donors (239pg/ml, 76.6–422) compared to controls (169.5pg/ml, 89–220pg/ml, p<0.05). Renin mRNA expression, and protein appeared qualitatively higher in the placental territory of the recipient compared to that of the donor and non-TTTS controls. We conclude that both fetuses in TTTS are exposed to high levels of RAS components; these appear to be produced from different sites, namely the kidney of the donor, and the placenta of the recipient. Given the markedly different phenotypes in the genetically identical fetuses with TTTS, we suggest that the source of RAS components may influence their clinical manifestations.
Copyright © 2008 Elsevier Ltd All rights reserved.

Keyword Monochorionic twins
Placenta
Renin angiotensin system
Twin–twin transfusion syndrome
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

 
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Created: Fri, 27 Mar 2009, 21:35:53 EST by Carmen Buttery on behalf of Faculty Of Health Sciences