Increased sodium-lithium countertransport in red cells of patients with Bartter's syndrome.

Erythrocyte sodium-lithium countertransport was evaluated in three adult patients with Bartter's syndrome, diagnosed on clinical and histopathological basis and on laboratory tests. As compared with age-matched control subjects, lithium effluxes to both sodium medium and to sodium-free medium were high in two patients and Na+-Li+ countertransport was significantly greater in all three patients. The relationship between increased Na+-Li+ countertransport and the proposed primary disorder of Bartter's syndrome (i.e., a primary tubular defect of chloride reabsorption) is not apparent. However, this finding favours the hypothesis of a generalized cellular membrane dysfunction of ion transport in Bartter's syndrome.