Late hyponatremia in premature infants: role of aldosterone and arginine vasopressin.

To assess the possible involvement of arginine vasopressin in the pathogenesis of late hyponatremia in preterm infants, serial measurements of sodium balance, fractional sodium excretion, plasma and urine osmolality and sodium concentration, and urinary aldosterone and arginine vasopressin excretion were performed at weekly intervals in nine healthy preterm infants. During the course of late hyponatremia, there was a significant increase in urinary aldosterone and arginine vasopressin excretion, from 0.94 +/- 0.16 to 4.30 +/- 0.76 micrograms/day and from 0.38 +/- 0.08 to 1.19 +/- 0.26 ng/day, respectively, from the first to the fourth to fifth weeks. A significant negative correlation was found between fractional sodium excretion and urinary aldosterone excretion. Aldosterone excretion, however, correlated positively with urinary arginine vasopressin excretion in seven of the nine infants. The parallel increase in urinary aldosterone and arginine vasopressin excretion in salt-losing premature infants may occur in response to the protracted contraction of the extracellular fluid compartment, and may contribute to the restoration of volume in the body fluid compartments and to the development of late hyponatremia.

Effects of maternal ritodrine administration on neonatal renal function.

Because of its effects on the cardiovascular and renin-angiotensin systems and on fluid and electrolyte homeostasis, maternal administration of ritodrine to inhibit preterm labor may cause significant alterations in renal function in the newborn infant. We determined inulin clearance, plasma renin activity, urinary arginine vasopressin excretion, and serum and urine electrolyte concentrations and osmolalities at 12 to 36 hours of life and at 6 days of life in 15 infants whose mothers had received ritodrine and in 15 infants whose mothers did not (control infants). At the time of each study, plasma ritodrine concentrations were obtained in the infants whose mothers received ritodrine. The infants whose mothers had received ritodrine had significantly lower inulin clearances and higher plasma renin activity and urinary arginine vasopressin excretion on day 1 but not on day 6. Gestational age was inversely correlated with plasma ritodrine concentration, plasma renin activity, and urinary arginine vasopressin excretion. There were no overt clinical signs of renal failure in any of the infants, and no differences in serum and urine electrolyte values, osmolality, fractional sodium excretion, or urine flow rate were observed between the groups.

Diuresis and respiratory distress syndrome: physiologic mechanisms and therapeutic implications.

Previous studies have suggested that spontaneous diuresis may be important to the recovery from respiratory distress syndrome in preterm infants. Daily quantification of fluid intake (1) and urine output (O) were recorded, and O/I and alveolar-arterial oxygen gradients (AaDO2) were determined for sequential eight-hour periods in 10 inborn premature infants with RDS. Sequential timed-urine-plasma collections were obtained during the first four days of life to evaluate the role of hormonal and vasoactive factors in the acute phase of RDS. Diuresis (O/I greater than 0.80) occurred at 25 to 32 hours, preceded any significant improvement in AaDO2 (which occurred at 57 to 64 hours), and was associated with a 6.2 +/- 1.4% decrease in body weight. Although there was no significant change in glomerular filtration rate, plasma AVP concentrations, or urinary excretion of AVP in the infants, there were significant decreases in both plasma concentrations and urinary excretion of 6-keto-PGF1 alpha (stable metabolite of prostacyclin) in sequential studies. These results suggest that changes in renal function or AVP may not be of primary importance in the diuresis associated with RDS, and that decreasing levels of prostacyclin, a prostaglandin that increases vascular permeability and lowers blood pressure, may have an important physiologic role.

Urinary prostaglandins, vasopressin, and kallikrein excretion in healthy children from birth to adolescence.

The urinary excretion of PGE2, PGF2 alpha, arginine-vasopressin, and kallikrein was measured in 58 healthy subjects aged 2 days to 13 years. In contrast to the activity of the renin-angiotensin-aldosterone system, which is known to decrease from birth, urinary excretion of PGE2, PGF2 alpha, vasopressin, and kallikrein significantly increased with age. These changes were not correlated to urine volume, natruresis, or glomerular filtration rate. Correction of the values by body surface area obliterated the differences for PGs and vasopressin, but not for kallikrein.