Developmental changes in renal tubular transport-an overview

Gattineni, Jyothsna; Baum, Michel

doi:10.1007/s00467-013-2666-6

Cited by 73Ion Transport and Channel RegulationRenal and related cancersAcute Kidney Injury Research

Developmental changes in renal tubular transport-an overview

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Gattineni, Jyothsna, Baum, Michel·2015·Pediatric Nephrology

DOI 10.1007/s00467-013-2666-6PMC PMC4028442

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Abstract

The adult kidney maintains a constant volume and composition of extracellular fluid despite changes in water and salt intake. The neonate is born with a kidney that has a small fraction of the glomerular filtration rate of the adult and immature tubules that function at a lower capacity than that of the mature animal. Nonetheless, the neonate is also able to maintain a constant extracellular fluid volume and composition. Postnatal renal tubular development was once thought to be due to an increase in the transporter abundance to meet the developmental increase in glomerular filtration rate. However, postnatal renal development of each nephron segment is quite complex. There are isoform changes of several transporters as well as developmental changes in signal transduction that affect the capacity of renal tubules to reabsorb solutes and water. This review will discuss neonatal tubular function with an emphasis on the differences that have been found between the neonate and adult. We will also discuss some of the factors that are responsible for the maturational changes in tubular transport that occur during postnatal renal development.

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All infants affected with classic CAH benefit from glucocorticoid plus adjunctive mineralocorticoid treatment at least within the first year of life.
“All infants affected with classic CAH benefit from glucocorticoid plus adjunctive mineralocorticoid treatment at least within the first year of life, when there is relative renal tubular resistance to the salt-retaining effects of aldosterone in early infancy (28) and low sodium content of infant diets (29).”
From Congenital Adrenal Hyperplasia—Current Insights in Pathophysiology, Diagnostics, and Management (2022) · cites this paper as [29]
The Cortical collecting duct section (page unavailable) reports resistance to aldosterone’s sodium-transport effect in neonatal rats, supporting the mechanism attached to citation (28). It does not establish that human infants with classic CAH benefit from combined treatment throughout the first year of life. (LLM, conf=0.84)
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[36]Schwartz GH Evan AP 1983 Development of solute transport in rabbit proximal tubule. I. HCO3 and glucose absorption Am J Physiol 245 F382 F390 6311027
[64]Baum M Quigley R 2004 Thyroid hormone modulates rabbit proximal straight tubule paracellular permeability Am J Physiol Renal Physiol 286 F477 F482 14644749 PMC4131928
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[165]Aperia A Larsson L Zetterstrom R 1981 Hormonal induction of Na-K-ATPase in developing proximal tubular cells Am J Physiol 241 F356 F360 6274204

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Congenital Adrenal Hyperplasia—Current Insights in Pathophysiology, Diagnostics, and Management
Claahsen - van der Grinten, H. L., Speiser, P. W., Ahmed, S. F., Arlt, W., Auchus, R. J., Falhammar, H., Flück, C. E., Guasti, L., Huebner, A., Kortmann, B. B. M., et al. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnab016 · Cited by 556 · see citing works

Authors: Gattineni, J., & Baum, M.
Affiliations: The University of Texas Southwestern Medical Center (US)
Corresponding author: Baum, Michel
ORCID: Gattineni, Jyothsna
Baum, Michel
Venue: Pediatric Nephrology
Publisher: Springer Science and Business Media LLC
Published: 2013-11-20
Volume: 30
Issue: 12
Pages: 2085-2098
ISSN: 0931-041X (ISSN-L)
1432-198X
DOI: 10.1007/s00467-013-2666-6
PMC: PMC4028442
OpenAlex: W2049706604
Cited by: 73
References: 170
Citations by year: 2026: 4 · 2025: 6 · 2024: 7 · 2023: 15 · 2022: 6 · 2021: 9 · 2020: 1 · 2019: 8 · 2018: 3 · 2017: 4 · 2016: 3 · 2015: 3 · 2014: 3
FWCI: 1.34
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.springer.com/tdm (tdm)
Locations: Pediatric Nephrology (publishedVersion, cc-by)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (KO8 DK089295, DK-41612, R01DK078596, T32DK007257, DK078596, R01DK041612, K08DK089295, P30DK079328, T32 DK 07257)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Renal and related cancers
Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
Keywords: renal tubular transport, neonatal kidney, transporter isoforms, signal transduction, glomerular filtration rate, extracellular fluid homeostasis, kidney maturation
MeSH terms: Animals, Biological Transport, Glomerular Filtration Rate, Humans, Kidney, Kidney Tubules, Sodium

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