In an attempt to provide information about the role of RAAS in development of late hyponatremia in low-birthweight neonates, simultaneous measurement of plasma renin activity, (PRA), plasma aldosterone concentration (PA), and urinary aldosterone excretion (UAE) was made using RIA methods along with determination of Na and K balance weekly up to the 6th week of life. Seven healthy male infants with mean birthweight of 1580 g, range: 1160–1850 g, and mean gestational age of 31 weeks, range: 30–32 weeks, were selected for the study.Summary
Due to the increased urinary Na loss, negative Na balance developed in the first 2 weeks followed by positive balance thereafter. PRA, PA, and UAE increased tremendously from the initially high values of 18.2 ± 4.1 ng/ml/hr, 1.7 ± 0.5 ng/ml, and 2.6 ± 0.4 μg/day, mean and SEM, to their maximum of 78.6 ± 18.1 ng/ml/hr, P < 0.01,6.8 ± 3.7 ng/ml, P < 0.05, and 26.4 ± 2.9 μg/day, P < 0.01, in the 3rd week, respectively. Later on, gradual declines occurred, however, PRA, PA, and UAE remained highly elevated even at the 6th week with values of 45.5 ± 15 ng/ml/hr, 1.6 ± 0.5 ng/ml, and 14.5 ± 1.4 μg/day, respectively.Summary
It is suggested that late hyponatremia of premature infants is due to tubular unresponsiveness to aldosterone and not to inadequate response of RAAS to stimulation.Speculation
The initially high urinary sodium excretion in premature infants is coupled with low urinary potassium excretion indicating limited renal sodium reabsorption in exchange for potassium. Later on, progressive increase in renal sodium-potassium exchange occurs and the plasma sodium and potassium concentrations gradually approach the normal values.Speculation
On the basis of these observations, one can assume the physiologic role of both the increasing activity of RAAS and also the increase in renal tubular responsiveness to aldosterone with advancing postnatal age.