Atrial natriuretic peptide mediated polyuria: pathogenesis of polyhydramnios in the recipient twin of twin-twin transfusion syndrome.

We studied the role of atrial natriuretic peptide (ANP) in the pathophysiology of polyhydramnios in monochorionic (MC) twins with and without twin-twin transfusion syndrome (TTTS). Matched maternal, fetal blood samples and amniotic fluids (AF) were obtained in utero (n=12) and at birth (n=20) from MC twins with TTTS. Blood and amniotic fluid samples were also collected from non-TTTS MC twin pairs in utero (n=6) and at birth (n=20). In both groups cellular localization of ANP in the fetal kidney and heart was performed using anti ANP rabbit polyclonal antibody. Concentrations of ANP in pg/ml were determined by radioimmunoassay.In recipient fetuses, ANP levels were higher than the donors both in utero (P< 0.001) and at birth (P< 0.001). No such differences were found between the non-TTTS twins. In the TTTS group maternal ANP levels were lower than the non-TTTS group (P< 0.05). A linear relationship was found between fetal ANP levels and the AF volumes removed at fetal blood sampling (r(2)=0.68;P< 0.01, n=12). ANP was localized predominantly to the cytoplasm of the distal convoluted tubules of the fetal kidney and heart, and the intensity of immunostaining for ANP in kidney and heart were markedly greater in the recipient than the donor twin. No such differences were found between the twin pairs. These data suggest that polyhdramnios in the recipient twin occurs as a consequence of ANP mediated increase in fetal urine output and raises the possibility of direct fetal therapy with ANP blocking agents. Copyright 2001 Harcourt Publishers Ltd.