Biological abnormalities simulating Bartter syndrome were observed in a preterm neonate with complex cyanotic congenital heart disease, for which ductus arteriosus was maintained open by high doses of prostaglandin (PG) until a Blalock shunt could be performed. These abnormalities spontaneously disappeared after cessation of PG administration. We postulate that the natriuretic effect of exogenous administered PG could further increase sodium wasting already induced by the cardiopathy thus leading to pseudo-Bartter syndrome.