Sodium excretion in normal and hypertensive pregnancy: a prospective study

One hundred fifty-eight intravenous saline solution infusions (3 mmol Na per kilogram body weight) were performed in (1) normal primigravid women during the second and third trimesters and post partum, after 1 week of either a high, low, or ad libitum salt intake; (2) normotensive primigravid women during midpregnancy who later developed pregnancy-induced hypertension, and (3) seven proteinuric and seven nonproteinuric primigravid women with ad libitum salt intake who had established pregnancy-induced hypertension. Sodium excretion did not differ significantly between pregnancy and after pregnancy despite marked differences in plasma renin activity, aldosterone concentration, volume, and glomerular filtration rate. Sodium excretion after saline solution loading varied according to prestudy sodium intake and was reduced between the second and third trimesters, independent of dietary salt intake. Those destined to develop pregnancy-induced hypertension had sodium excretion similar to that of continuously normotensive subjects during the second trimester, but those with established proteinuric pregnancy-induced hypertension had the lowest plasma volume, plasma aldosterone concentration, and plasma renin activity and retained sodium to the same degree as salt-deplete women with normotension. These results demonstrate that the balance of sodium regulatory factors is similar between pregnancy and post partum, that prestudy salt intake and stage of gestation can alter the natriuretic response to saline solution loading, and that normal pregnant women retain more administered sodium in late pregnancy than in midpregnancy despite further increases in plasma volume and no alterations to blood pressure or glomerular filtration rate. Those with established proteinuric pregnancy-induced hypertension retain sodium avidly without stimulation of plasma renin activity or plasma aldosterone concentration, findings not apparent during midpregnancy in those who later developed this disorder.