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Pathogenesis of Twin-Twin Transfusion Syndrome: The Renin-Angiotensin System Hypothesis

Mahieu-Caputo D.a · Muller F.e · Joly D.b · Gubler M.-C.c · Lebidois J.d · Fermont L.d · Dumez Y.a · Dommergues M.a

Author affiliations

Departments of aObstetrics, bNephrology and cINSERM U423, dPaediatric Cardiology, Hôpital Necker-Enfants Malades, AP-HP and University Paris V, and eBiochemistry Laboratory, Hôpital Ambroise Paré, Boulogne, AP-HP and University Paris V, Paris, France

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Fetal Diagn Ther 2001;16:241–244

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: June 07, 2001
Issue release date: July – August

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 1015-3837 (Print)
eISSN: 1421-9964 (Online)

For additional information: https://www.karger.com/FDT

Abstract

In spite of active perinatal management, twin-twin transfusion syndrome (TTTS) remains a severe disease with a high risk of neonatal mortality and morbidity. TTTS initially results from an unbalanced blood flow from a donor to a recipient twin. However, its pathogenesis remains unclear, although cardiovascular disturbances and regulation of fetal volemia and diuresis seem central in this syndrome. Previously, we demonstrated that the renin-angiotensin system (RAS) was up-regulated in donor twins as a consequence of hypovolemia, and down-regulated in recipients. This was the first evidence of the implication of the RAS in TTTS. We hypothesize that the RAS plays a key role in the pathogenesis of TTTS. In the donor, RAS up-regulation aggravates oligohydramnios and may increase arterial resistance, which could contribute to placental dysfunction leading to intrauterine growth restriction. In the recipient, paradoxical RAS activation, due to transfer of effectors such as angiotensin II through placental shunts, could explain fetal vascular disturbances and cardiomyopathy. According to our hypothesis, TTTS would appear similar to the classical model of hypertension referred to as ‘2 kidneys-1 clip’ with a donor twin, comparable to the clipped kidney, intoxicating its cotwin, comparable to the normal kidney.

© 2001 S. Karger AG, Basel


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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: June 07, 2001
Issue release date: July – August

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 1015-3837 (Print)
eISSN: 1421-9964 (Online)

For additional information: https://www.karger.com/FDT


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