Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: An explanation for cardiovascular disturbances in the recipient

Mahieu-Caputo, Dominique, Meulemans, Alain, Martinovic, Jelena, Gubler, Marie-Claire, Delezoide, Anne-Lise, Muller, Francoise, Madelenat, Patrick, Fisk, Nicholas M. and Dommergues, Marc (2005) Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: An explanation for cardiovascular disturbances in the recipient. Pediatric Research, 58 4: 685-688. doi:10.1203/01.PDR.0000180558.03164.E8


Author Mahieu-Caputo, Dominique
Meulemans, Alain
Martinovic, Jelena
Gubler, Marie-Claire
Delezoide, Anne-Lise
Muller, Francoise
Madelenat, Patrick
Fisk, Nicholas M.
Dommergues, Marc
Title Paradoxic activation of the renin-angiotensin system in twin-twin transfusion syndrome: An explanation for cardiovascular disturbances in the recipient
Journal name Pediatric Research   Check publisher's open access policy
ISSN 0031-3998
1530-0447
Publication date 2005-10
Sub-type Article (original research)
DOI 10.1203/01.PDR.0000180558.03164.E8
Volume 58
Issue 4
Start page 685
End page 688
Total pages 4
Place of publication Baltimore, MD, U.S.A.
Publisher Lippincott, William & Wilkins
Language eng
Subject 111401 Foetal Development and Medicine
111402 Obstetrics and Gynaecology
1114 Paediatrics and Reproductive Medicine
Formatted abstract
Despite advances in treatment, twin-to-twin transfusion syndrome (TTTS) still carries a high risk for perinatal mortality and morbidity. Simple blood transfer from the donor to the recipient twin cannot explain all of the features of this disease, in particular the recipient's hypertensive cardiomyopathy. We report a case in which TTTS resulted in preterm delivery with early neonatal death of both twins, allowing assessment of the renin angiotensin system (RAS) status of each fetus, both by cord blood renin and aldosterone assay and by renal immunohistochemistry. The donor had severe oliguria/oligohydramnios, whereas the recipient, in addition to severe polyuria/polyhydramnios, had cardiomyopathy, atrioventricular regurgitation, and ascites. Although immunohistochemistry demonstrated that renal secretion of renin was up-regulated in the donor and down-regulated in the recipient, cord blood levels of renin and aldosterone were similar, with high renin levels in both twins. This observation supports the hypothesis that despite renal RAS down-regulation, the recipient is exposed to RAS effectors elaborated in the donor and transferred via placental shunts. This may contribute to cardiomyopathy and hypertension in the recipient, which cannot be accounted for by hypervolemia alone. We thus hypothesized that in TTTS, the recipient's hypertensive cardiomyopathy could be due to a mechanism similar to the classical model of hypertension referred to as 2 kidneys-1 clip. Thus the hypovolemic donor twin, comparable to the clipped kidney, produces vasoactive hormones that compromise the recipient, comparable to the normal kidney, causing hypertension and cardiomyopathy.
Copyright © 2005 International Pediatric Research Foundation, Inc.

Keyword Twin-to-twin transfusion syndrome
Renin-angiotensin system
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Fri, 20 Mar 2009, 15:16:59 EST by Maria Campbell on behalf of Faculty Of Health Sciences