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 coarse 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 t~g/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. (J PeDIATR 106:990, 1985) E. Sulyok, M.D., L. Kov~cs, M.D., B. Lichardus, M.D., N. Michajlovskij, M.D., V. Lehotska, M.D., V. N61nethova, M.D., L. Varga, M.D., and T. Ertl, M.D. Pbcs, Hungary, and Bratislava, Czechoslovakia THE LIMITED ABILITY of the immature kidney to reab- sorb sodium results in renal salt wasting, negative sodium balance, and a decline in plasma sodium concentration in low birth weight premature infants, v6 The pathogenesis of the "late hyponatremia" is not established,4 although evidence has been provided that, in response to the sodium depleted state, adaptive endocrine changes occur to restore sodium balance. 3,7 Renal immaturity, however, impairs efficient tubular sodium reabsorption, so that urinary sodium loss continues, 6,8 and protracted contraction of body fluid compartments can be anticipated. Studies in preterm infants with late hyponatremia have failed to reveal any alterations in total body water and extracellular fluid compartments, 4 thus raising the possi- From the Department of Obstetrics and Gynecology, University Medical School, Pecs; and the 2nd Department of Pediatrics, Comenius University, and the Institute of Experimental Endocri- nology, Slovak Academy of Sciences, Bratislava. Submitted for publication Aug. 10, 1984; accepted Nov. 27, 1984. Reprint requests: E. Sulyok, M.D., Department of Obstetrics and Gynecology, University Medical School, 7624 Pbcs, Hungary. bility that, in addition to the highly activated renin- angiotensin-aldosterone system, other endocrine systems may be involved in the maintenance of the volume of body fluids. In support of this possibility is the fact that the neonatal neurohypophysis is readily responsive to stimula- tion; 9~2 consequently, the sodium and volume depletion resulting from the renal salt wasting may induce signifi- cant elevation in arginine vasopressin secretion, which in turn may enhance renal water reabsorption to restore the volume of body fluids to normal. I AVP Arginine vasopressin [ In an attempt to provide information about the possible involvement of AVP in the development of late hypona- tremia in LBW preterm infants, we determined urinary AVP excretion, sodium balance, and aldosterone excretion during the course of hyponatremia. METHODS Nine healthy preterm infant boys were selected for the study. They ranged in birth weight from 1020 to 1620 gm (mean 1372 gin) and in gestational age from 29 to 33 990 TheJournalofPEDIATRICS