INFLUENCE OF NACL SUPPLEMENTATION ON VASOPRESSIN SECRETION AND WATER-EXCRETION IN PREMATURE-INFANTS

The study was carried out to assess the possible involvement of excess AVP and free water retention in the development of late hyponatremia by comparing the postnatal course of plasma AVP and urinary excretion of AVP and sodium as well as creatinine, osmolar and free water clearances in premature infants with (group S) and without (group NS) NaCl supplementation. Plasma total protein and albumin concentrations were also determined. Group NS consisted of 8 infants with a birth weight of 1, 1 50-1,730 g (mean: 1,440 g) and gestational age of 28-32 weeks (mean: 30.4 weeks). Group S included 8 infants with a mean birth weight of 1,390 g (range: 980-1,700 g) and a mean gestational age of 30.1 weeks (range: 27-32 weeks). Measurements were made on the 7th day and weekly thereafter until the 5th week of life. NaCl supplementation was given in a dose of 3-5 and 1.5-2.5 mmol/kg/day for 8-21 and 22-35 days, respectively. Infants receiving sodium supplements had significantly greater urinary sodium excretion (p < 0.0 1), retained more sodium (p < 0.0 1), maintained plasma sodium at normal levels and gained weight at slightly higher rates when compared with those on low sodium. Plasma AVP tended to be higher in group S but did not differ significantly from that in NS group. Urinary AVP excretion, however, either expressed in ng/day or ng/100 ml GFR, was significantly higher in group S, although the age-related increase could not be seen when correction was made for GFR. The respective values of AVP excretion in weeks 1, 2-3 and 4-5 were 1.02 +/- 0.17, 3.19 +/- 0.47 and 2.44 +/- 0.22 ng/day in group S and 0.60 +/- 0.12, 0.96 +/- 0.12 (p < 0.001) and 1.61 +/- 0.26 ng/day (p < 0.01) in group NS. NaCl supplementation and the increased AVP excretion was associated with significant decreases in GFR (p < 0.05), free water excretion (p < 0.01), plasma total protein (p < 0.0 1) and plasma albumin (p < 0.0 1) concentrations. These data suggest that NaCl supplementation prevents late hyponatremia at the expense of AVP-mediated water retention and subsequent volume expansion.