Clinical and Experimental Nephrology

, Volume 14, Issue 5, pp 518–519 | Cite as

Clinical improvement in patients with autosomal recessive pseudohypoaldosteronism and the necessity for salt supplementation

  • Aaron HanukogluEmail author
  • Israel Hanukoglu
Letter to the Editor


Pseudohypoaldosteronism Aldosterone Epithelial sodium channel ENaC Salt supplementation Electrolyte regulation Na–Cl cotransporter 


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    Adachi M, Asakura Y, Muroya K, Tajima T, Fujieda K, Kuribayashi E, Uchida S. Increased Na reabsorption via the Na–Cl cotransporter in autosomal recessive pseudohypoaldosteronism. Clin Exp Nephrol. 2010;14:228–32.CrossRefPubMedGoogle Scholar
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    Hanukoglu A, Edelheit O, Shriki Y, Gizewska M, Dascal N, Hanukoglu I. Renin-aldosterone response, urinary Na/K ratio and growth in pseudohypoaldosteronism patients with mutations in epithelial sodium channel (ENaC) subunit genes. J Steroid Biochem Mol Biol. 2008;111:268–74.CrossRefPubMedGoogle Scholar
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    Edelheit O, Hanukoglu I, Shriki Y, Tfilin M, Dascal N, Gillis D, Hanukoglu A. Truncated beta epithelial sodium channel (ENaC) subunits responsible for multi-system pseudohypoaldosteronism support partial activity of ENaC. J Steroid Biochem Mol Biol. 2010;119:84–8.CrossRefPubMedGoogle Scholar
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    Hanukoglu A. Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects. J Clin Endocrinol Metab. 1991;73:936–44.CrossRefPubMedGoogle Scholar
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    Porter J, Kershaw M, Kirk J, Trevelyan N, Shaw NJ. The use of sodium resonium in pseudohypoaldosteronism. Arch Dis Child. 2003;88:1138–9.CrossRefPubMedGoogle Scholar

Copyright information

© Japanese Society of Nephrology 2010

Authors and Affiliations

  1. 1.Department of PediatricsTel Aviv University, Sackler Medical SchoolTel AvivIsrael
  2. 2.Division of Pediatric EndocrinologyE. Wolfson Medical CenterHolonIsrael
  3. 3.Department of Molecular BiologyAriel University CenterArielIsrael

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