Abstract
Since learning that glomerular filtration rate (GFR) during the first six months of life could not be factored for body size to be comparable with normal adult values (1), renal function in newborn infants has been considered limited. When 10% sodium chloride was fed to normal subjects, urine flow rate did not increase as much in infants as it did in adults; a conclusion was that sodium excretion in the infants was impaired even though no measurements of sodium had been made (2). When a developmental study of the newborn kidney’s capacity to excrete water was performed, newborn infants excreted a greater fraction of an oral water load with each successive postnatal day, but the ability to excrete the water like an adult kidney was not observed during the first two weeks of life (3). The notion followed that the diluting mechanism of the neonatal kidney was limited compared to the adult kidney. When challenged by hydropenia, the inability of the neonatal kidney to concentrate urine to 1200 mOsm/kg like the adult kidney was further evidence of limited renal function in the neonate (4).
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References
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© 1986 Martinus Nijhoff Publishing, Boston
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Arant, B.S. (1986). Functional Immaturity of the Newborn Kidney—Paradox or Prostaglandin?. In: Strauss, J. (eds) Homeostasis, Nephrotoxicity, and Renal Anomalies in the Newborn. Developments in Nephrology, vol 11. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2637-3_19
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DOI: https://doi.org/10.1007/978-1-4613-2637-3_19
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