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[Fetal polyuria and decrease of electrolytes in amniotic fluid as principal markers of neonatal Bartter's syndrome].

The above mentioned after a careful investigation of the modern pathogenic aspects of Bartter's syndrome, evaluated the markers that are useful for the prenatal diagnosis of Bartter's syndrome, they pointed out, as in both cases the presence of polyhydramnios not associated with ecographically detectable fetal malformations, elevated chloride in the amniotic fluid, accompanied in one case by increased levels of aldosterone, in the other case by the increase of K, as being reliable markers for the prenatal diagnosis of these conditions.

Amniotic Fluid↗

The mechanism of polyuria in rats pretreated with lithium studies by in vitro microperfusion.

The collecting ducts in papillae taken from normal rats have a measurable increase in diffusional tritiated water (THO) permeability with ADH 5 mu unit/ml and this increase is maximal with antidiuretic hormone (ADH) 100 mu unit/ml added to media. The presence of plasma from rats pretreated with lithium to make them polyuric inhibited the response to ADH. The lowest concentration of ADH that caused a measurable increase in diffusional water permeability was 50 mu unit/ml and the increase was maximal with ADH 2000 mu unit/ml. The maximum response to ADH did not differ whether plasma from control or lithium pretreated rats was used. However, the dose-response curve to ADH was shifted to the right by the plasma from lithium-pretreated rats. Lithium added to the plasma from control rats did not alter the response to ADH. It is proposed that lithium given to rats causes a circulatory factor to be produced that inhibits in a competitive fashion the response of the collecting duct to ADH. Such an effect would explain many features of the impairment of water excretion associated with lithium use.

Animals↗