Low renal mineralocorticoid receptor expression at birth contributes to partial aldosterone resistance in neonates
Open accessAbstract
The human neonatal period is characterized by renal immaturity with impaired capacity to regulate water and sodium homeostasis, resembling partial aldosterone resistance. Because aldosterone effects are mediated by the mineralocorticoid receptor (MR), we postulated that this hormonal unresponsiveness could be related to low MR expression in the distal nephron. We measured aldosterone and renin levels in umbilical cord blood of healthy newborns. We used quantitative real-time PCR and immunohistochemistry to analyze the expression of MR and key players of the mineralocorticoid signaling pathway during human and mouse renal development. High aldosterone and renin levels were found at birth. MR mRNA was detected in mouse kidney at d 16 postcoitum, peaking at d 18 postcoitum, but its expression was surprisingly very low at birth, rising progressively afterward. Similar biphasic temporal expression was observed during human renal embryogenesis, with a transient expression between 15 and 24 wk of gestation but an undetectable immunoreactive MR in late gestational and neonatal kidneys. This cyclic MR expression was tightly correlated with the evolution of the 11beta-hydroxysteroid dehydrogenase type 2 and the epithelial sodium channel alpha-subunit. In contrast, glucocorticoid and vasopressin receptors and aquaporin 2 followed a progressive and sustained evolution during renal maturation. Our study provides the first evidence for a low renal MR expression level at birth, despite high aldosterone levels, which could account for compromised postnatal sodium handling. Elucidation of regulatory mechanisms governing MR expression should lead to new strategies for the management of sodium waste in preterms and neonates.
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These patients may recover spontaneously and grow to adulthood without therapy, probably reflecting the increasing sensitivity to mineralocorticoid action and sodium intake with advancing age.
“These patients may recover spontaneously and grow to adulthood without therapy, probably reflecting the increasing sensitivity to mineralocorticoid action and sodium intake with advancing age (480, 481) (Fig. 11).”
From The Molecular Biology, Biochemistry, and Physiology of Human Steroidogenesis and Its Disorders (2011) · cites this paper as [481]
The Discussion (page not available in our copy) reports that renal mineralocorticoid receptor levels rise after birth as the kidney matures, supporting an age-related change in mineralocorticoid responsiveness. It does not say that patients recover spontaneously or reach adulthood without therapy, nor does it establish increasing sodium intake with age as the reason. Instead, it says salt wasting in children with PHA1a can be rescued by sodium supplementation. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe need for mineralocorticoids decreases with age, as serum aldosterone is high and renal mineralocorticoid receptor mRNA is low at birth, and the salt content in most diets is high.
“The need for MCs decreases with age, as serum aldosterone is high and renal MC receptor mRNA is low at birth (204), and the salt content in most diets is high.”
From Congenital Adrenal Hyperplasia Due to Steroid 21-Hydroxylase Deficiency: An Endocrine Society* Clinical Practice Guideline (2018) · cites this paper as [204]
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Preterm birth is associated with epigenetic programming of transgenerational hypertension in mice
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Self-citationmiR-324-5p and miR-30c-2-3p Alter Renal Mineralocorticoid Receptor Signaling under Hypertonicity
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Adrenal Hypoplasia Congenita Presenting as Congenital Adrenal Hyperplasia
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Model-Informed Dose Optimization of Spironolactone in Neonates and Infants
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Neonatal Pseudohypoaldosteronism Type-1 in Japan
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Corticosterone Methyl Oxidase Type 1 (CMO1) Deficiency Due to CYP11B2 Mutation: Two Case Reports
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Renal Aspects of Sodium Metabolism in the Fetus and Neonate
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Salt supplementation ameliorates developmental kidney defects in COX-2−/− mice
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A Novel Mutation of theCYP11B2in a Saudi Infant with Primary Hypoaldosteronism
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Early urinary aldosterone excretion in very low birth weight infants
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Renal pseudohypoaldosteronism type 1—an adult case series including a novel gene variant
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Fluid and Electrolyte Physiology in the Fetus and Neonate
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Fluid and Electrolyte Management of High-Risk Infants
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Résistances aux hormones stéroïdes : physiologie et pathologie
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Compliance Issues in Managing 21 Hydroxylase Deficiency and their Short/Long-Term Consequences
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Dynamics of Renal Electrolyte Excretion in Growing Mice
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Renal Aspects of Sodium Metabolism in the Fetus and Neonate
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Impact of aldosterone deficiency on the development of diuretic resistance in mice
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Postnatal Changes of Renin and Aldosterone in Term and Preterm Infants from Birth to Day 5
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- Authors
- Martinerie, L., Viengchareun, S., Delezoide, A.-L., Jaubert, F., Sinico, M., Prevot, S., Boileau, P., Meduri, G., & Lombès, M.
- Affiliations
- Institut National de la Santé et de la Recherche Médicale (L.M., S.V., G.M., M.L.), Unité 693, Le Kremlin-Bicêtre F-94276, France
- Université Paris-Sud (FR)
- Assistance Publique – Hôpitaux de Paris (FR)
- Hôpital Necker-Enfants Malades (FR)
- Hôpital Intercommunal de Créteil (FR)
- et de Pédiatrie et Réanimation Néonatales (P.B.), Clamart F-92141, France
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2009-05-28
- Volume
- 150
- Issue
- 9
- Pages
- 4414-4424
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3201843
- OpenAlex
- W2159132227
- Semantic Scholar
- 247e04eb6c5c516750184b5faf42d5b661255770
- Cited by
- 97
- References
- 45
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 6 · 2023: 7 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 11 · 2016: 7 · 2015: 3 · 2014: 4 · 2013: 6 · 2012: 7
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Pfizer
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- mineralocorticoid receptor, kidney development, umbilical cord blood, aldosterone, renin, 11β-hydroxysteroid dehydrogenase type 2, epithelial sodium channel, aquaporin-2, sodium homeostasis, preterm infants
- MeSH terms
- Aldosterone, Animals, Drug Resistance, Female, Humans, Infant, Newborn, Kidney, Male, Receptors, Glucocorticoid, Renin, Renin-Angiotensin System, Receptors, Vasopressin, Receptors, Mineralocorticoid, 11-beta-Hydroxysteroid Dehydrogenase Type 2, Mice, Aquaporin 2, Epithelial Sodium Channels
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