Key result
Recipient twins in severe twin transfusion syndrome show elevated cord blood ANF versus donor twins.
Case Report (n=3)
Elevated ANF release from the fetal heart in recipient twins provides a pathophysiological mechanism for polyhydramnios in severe twin transfusion syndrome.
Does not yet alter TTTS management; extends mechanistic insights into polyhydramnios and warrants prospective validation.
In 3 cases of severe twin transfusion syndrome we demonstrate that the concentration of atrial natriuretic factor (ANF) in the cord blood of recipient twins is significantly elevated compared to that of donor twins. The discrepancy between recipient and donor concentration correlates with the volume of transfusion. The following pathophysiological mechanism for explaining polyhydramnios in recipient twins is proposed: chronic overload in recipient twins causes enhanced release of ANF from the fetal heart. Consequently, increased fetal urine production leads to polyhydramnios, which is additionally enhanced by inhibition of ADH release.
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Wieacker et al. (2009) conducted a case report in severe twin transfusion syndrome (n=3). Recipient twin status vs. Donor twin status was evaluated on concentration of atrial natriuretic factor (ANF) in cord blood. Recipient twins in severe twin transfusion syndrome had significantly elevated cord blood concentrations of atrial natriuretic factor compared to donor twins.
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