title: Sodium and potassium clearances by the maturing kidney: clinical-molecular correlates.
abstract: A temporal dissociation exists between the early appearance of sodium absorptive and later detection of potassium secretory processes in the maturing rabbit collecting duct. To extend the latter findings to the human, we sought to correlate developmental changes in renal sodium and potassium clearances with the molecular expression of corresponding ion channels in kidneys of premature infants. In a longitudinal prospective study of 23- to 31-week gestational age (GA) infants, sodium, potassium, and creatinine clearances were measured weekly for 5 weeks and the absolute and fractional excretions of sodium (FE(Na)) and potassium (FE(K)) calculated. Gene-specific probes were used to assess steady-state abundance of mRNA encoding the sodium channel ENaC and potassium channel ROMK in homogenates of human kidneys (obtained from the Anatomic Gift Foundation). Although urinary losses of sodium in infants <approximately 28 weeks GA exceeded intake, leading to a state of negative sodium balance, most infants >/=28 weeks and all infants >approximately 32 weeks GA achieved a state of positive balance, a maturational process associated with a decrease in FE(Na )and increase in ENaC. Infants >approximately 30 weeks GA maintained a state of positive potassium balance. We noted a twofold reduction in FE(K )after approximately 26 weeks GA and no change in ROMK abundance during the developmental window studied. We speculate that the developmental regulation of renal ENaC expression contributes, at least in part, to the decrease in FE(Na )observed with advancing GA, and that in the human, as in the rabbit, there is a delay between the maturation of sodium absorptive and potassium secretory pathways.
authors.affiliation: Division of Neonatology, Mount Sinai School of Medicine, New York, NY 10029, USA.
authors.forename: Mercedes M
authors.initials: MM
authors.lastname: Delgado
authors.forename: Rajeev
authors.initials: R
authors.lastname: Rohatgi
authors.forename: Shahana
authors.initials: S
authors.lastname: Khan
authors.forename: Ian R
authors.initials: IR
authors.lastname: Holzman
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Satlin
mesh_terms: D003404:Creatinine / Q000378:metabolism; D053503:Epithelial Sodium Channels; D005260:Female; D015870:Gene Expression; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000378:metabolism*; D007668:Kidney / Q000254:growth & development* / Q000378:metabolism*; D008137:Longitudinal Studies; D008297:Male; D009399:Nephrons / Q000254:growth & development / Q000378:metabolism; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000235:genetics; D024661:Potassium Channels, Inwardly Rectifying; D011446:Prospective Studies; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000235:genetics; D014882:Water-Electrolyte Balance / Q000502:physiology
chemical_list: D053503:Epithelial Sodium Channels; C086989:KCNJ1 protein, human; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D015222:Sodium Channels; D012964:Sodium; D003404:Creatinine; D011188:Potassium