2, 8 Using published measures of glomerular and tubular function in preterm infants, we modeled expected urine sodium losses and urine sodium concentrations with advancing gestational and postnatal ages. However, in the preterm population, an approach using urine sodium concentrations as an indicator of total body sodium status is confounded by renal tubular immaturity and higher obligatory urine sodium losses, as well as ongoing maturation of renal function with postnatal age. 7 In the mature kidney, a low urine sodium concentration often reflects active renal conservation of sodium in response to a decrease in total body sodium. 3– 6Īn underappreciated though convenient approach to the assessment of sodium homeostasis is the use of urine sodium concentration measured from a spot urine sample. 1, 2 The issue of determining the quantity of sodium that preterm infants require is significant given the impact of total body sodium status on somatic growth and the well-described link between postnatal growth failure and adverse neurodevelopmental outcome. Beyond the immediate postnatal period, preterm infants have higher sodium requirements (mEq/kg) than term infants and older children, primarily related to the inability of the preterm kidney to retain salt. Preterm birth poses a unique challenge to this process as the immature kidney lacks fully functional regulatory systems, including those involved in sodium homeostasis. Responsibility for maintaining the composition of extracellular fluid with respect to constituents other than oxygen and carbon dioxide resides largely with the kidneys. Sodium is the major cation of extracellular fluid, which includes blood plasma and interstitial fluid.
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