Authors: Mercedes M Delgado Rajeev Rohatgi Shahana Khan Ian R Holzman Lisa M Satlin
Publish Date: 2003/06/17
Volume: 18, Issue: 8, Pages: 759-767
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 31week gestational age GA infants sodium potassium and creatinine clearances were measured weekly for 5 weeks and the absolute and fractional excretions of sodium FENa and potassium FEK calculated Genespecific probes were used to assess steadystate 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 ~28 weeks GA exceeded intake leading to a state of negative sodium balance most infants ≥28 weeks and all infants ~32 weeks GA achieved a state of positive balance a maturational process associated with a decrease in FENa and increase in ENaC Infants ~30 weeks GA maintained a state of positive potassium balance We noted a twofold reduction in FEK after ~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 FENa 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 pathwaysThe authors gratefully acknowledge Beth Zavilowitz for her expert technical assistance Dr Patricia Wilson Mount Sinai School of Medicine for generously providing us with human nephrectomy specimens and Dr Adrian Spitzer Albert Einstein College of Medicine for his insightful review of the manuscript This work was supported by grants from the National Institutes of Health DK38470 and DK64104 and the Polycystic Kidney Disease Foundation LMS RR was supported by a National Kidney Foundation Fellowship Grant An abstract of this work was presented at the 2000 Annual Meetings of the Eastern Society of Pediatric Research Atlantic City NJ USA and Academic Pediatric Societies Boston Mass USA
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