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PEDIATRICS Vol. 106 No. 3 September 2000, pp. 561-567

Effect of Prenatal Steroids on Potassium Balance in Extremely Low Birth Weight Neonates

Received Apr 13, 1999; accepted Dec 22, 1999.

Said A. Omar*, Dagger , Joseph D. DeCristofaro§, Bajrang I. Agarwal, and Edmund F. LaGammaparallel

From the * Department of Pediatrics and Human Development, Michigan State University, East Lansing, Michigan; Dagger  Sparrow Health System, Lansing, Michigan; § Department of Pediatrics, University Hospital, Stony Brook, New York; parallel  Department of Pediatrics, Westchester Medical Center, Valhalla, New York; and  Department of Pediatrics, Lawrence Hospital, Westchester, New York.

Objective.  Potassium is the most abundant intracellular cation and plays an important role in a variety of cell functions. Potassium homeostasis and regulation are important aspects of fluid and electrolyte homeostasis in extremely low birth weight (ELBW) infants. Because prenatal steroid (PNS) treatment promotes maturation of many epithelial cell systems, we sought to determine whether PNS affects potassium homeostasis in ELBW infants (<1000 g) during the first week of life.

Method.  Serum potassium (SK) concentration, potassium intake and output, and renal clearance were collected prospectively each day during the first week of life. Infants whose mothers received a full course of steroids before delivery (PNS group: n = 16) were compared with those infants whose mothers did not receive steroids (nonsteroid group [NSG]: n = 14). The decision to treat with PNS was made entirely by the obstetric staff in a nonrandomized manner. Potassium intake and excretion and serum and urine electrolytes were measured every 12 hours, and urine output was monitored every 2 to 3 hours. Hyperkalemia was defined as SK >6.5 mmol/L in a nonhemolyzed sample on at least 1 measurement from a central line.

Results.  There were no significant differences between the groups in gestational age, Apgar score, and birth weight. SK increased initially after birth in the absence of exogenous K intake in all infants, then subsequently decreased and stabilized by day 4 of life. The peak SK was significantly lower in the PNS group than in the NSG group (5.2 ± .2 mmol/L vs 6.2 ± .4 mmol/L). Moreover, the peak SK was higher than 6.5 mmol/L in 70% of the NSG infants and in none of the PNS group. Hyperkalemia occurred in the NSG infants within the first 2 days when urine output was significantly lower than in PNS infants. SK peaked in the absence of potassium intake with similar potassium excretion in both groups. PNS infants had similar cumulative potassium intake with a lower cumulative potassium excretion than did NSG infants. PNS infants had a significantly less negative potassium balance than did NSG infants by day 7 of life (-1.0 mmol/kg vs -7.0 mmol/kg). There was no statistical difference in the daily serum creatinine levels, fractional excretion of potassium, and in the daily creatinine clearance between the 2 groups.

Conclusion.  We conclude that treatment with PNS prevents the nonoliguric hyperkalemia known to occur in ELBW neonates. We speculate that PNS induces upregulation of cell membrane sodium, potassium-adenosinetriphosphatase activity in the fetus. The differences in negative potassium balance may be accounted for by stabilization of cell membranes that may result in a decrease in potassium shift from intracellular to extracellular compartments.  Key words:  hyperkalemia, potassium balance, fluid homeostasis, prenatal steroids, creatinine clearance.




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