Literature DB >> 23689903

CUL3 gene analysis enables early intervention for pediatric pseudohypoaldosteronism type II in infancy.

Madori Osawa1, Yumi Ogura, Kiyoshi Isobe, Shinichi Uchida, Shigeaki Nonoyama, Hiroyuki Kawaguchi.   

Abstract

BACKGROUND: Four genes responsible for pseudohypoaldosteronism type II (PHA-II) have been identified, thereby facilitating molecular diagnostic testing. CASE-DIAGNOSIS/TREATMENT: A 1-year-old boy with prolonged hyperkalemia, metabolic acidosis, hyperchloremia, growth delay, and mild hypertension was diagnosed with PHA-II based on the detection of exon 9 skipping in CUL3 mRNA. The impaired splicing was the result of a de novo, previously unreported single nucleotide substitution in the splice acceptor site of CUL3 intron 8. Among the four genes reported to be involved in PHA-II, CUL3 was the primary suspect in our patient because in patients with the CUL3 mutation, the onset of disease is often early in infancy and the phenotypes of PHA-II are more severe. Our patient was treated with trichlormethiazide, which inhibits the function of the sodium-chloride co-transporter (NCC), and the outcome was favorable, with correction of body fluids and blood electrolyte homeostasis.
CONCLUSION: Since chronic acidosis and hypertension associated with PHA-II can result in delayed growth and development in pediatric patients, genetic analysis to detect the CUL3 mutation and to enable intervention early in the disease course would be beneficial for infants with suspected PHA-II.

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Year:  2013        PMID: 23689903     DOI: 10.1007/s00467-013-2496-6

Source DB:  PubMed          Journal:  Pediatr Nephrol        ISSN: 0931-041X            Impact factor:   3.714


  6 in total

1.  Chronic acidosis-induced growth retardation is mediated by proton-induced expression of Gs protein.

Authors:  Ruth Goldberg; Ella Reshef-Bankai; Raymond Coleman; Jacob Green; Gila Maor
Journal:  J Bone Miner Res       Date:  2006-05       Impact factor: 6.741

2.  Phenotypes of pseudohypoaldosteronism type II caused by the WNK4 D561A missense mutation are dependent on the WNK-OSR1/SPAK kinase cascade.

Authors:  Motoko Chiga; Fatema H Rafiqi; Dario R Alessi; Eisei Sohara; Akihito Ohta; Tatemitsu Rai; Sei Sasaki; Shinichi Uchida
Journal:  J Cell Sci       Date:  2011-04-12       Impact factor: 5.285

3.  Human hypertension caused by mutations in WNK kinases.

Authors:  F H Wilson; S Disse-Nicodème; K A Choate; K Ishikawa; C Nelson-Williams; I Desitter; M Gunel; D V Milford; G W Lipkin; J M Achard; M P Feely; B Dussol; Y Berland; R J Unwin; H Mayan; D B Simon; Z Farfel; X Jeunemaitre; R P Lifton
Journal:  Science       Date:  2001-08-10       Impact factor: 47.728

4.  Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone insensitivity in humans.

Authors:  M Brüngger; H N Hulter; R Krapf
Journal:  Kidney Int       Date:  1997-01       Impact factor: 10.612

5.  Molecular pathogenesis of pseudohypoaldosteronism type II: generation and analysis of a Wnk4(D561A/+) knockin mouse model.

Authors:  Sung-Sen Yang; Tetsuji Morimoto; Tatemitsu Rai; Motoko Chiga; Eisei Sohara; Mayuko Ohno; Keiko Uchida; Shih-Hua Lin; Tetsuo Moriguchi; Hiroshi Shibuya; Yoshiaki Kondo; Sei Sasaki; Shinichi Uchida
Journal:  Cell Metab       Date:  2007-05       Impact factor: 27.287

6.  Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities.

Authors:  Lynn M Boyden; Murim Choi; Keith A Choate; Carol J Nelson-Williams; Anita Farhi; Hakan R Toka; Irina R Tikhonova; Robert Bjornson; Shrikant M Mane; Giacomo Colussi; Marcel Lebel; Richard D Gordon; Ben A Semmekrot; Alain Poujol; Matti J Välimäki; Maria E De Ferrari; Sami A Sanjad; Michael Gutkin; Fiona E Karet; Joseph R Tucci; Jim R Stockigt; Kim M Keppler-Noreuil; Craig C Porter; Sudhir K Anand; Margo L Whiteford; Ira D Davis; Stephanie B Dewar; Alberto Bettinelli; Jeffrey J Fadrowski; Craig W Belsha; Tracy E Hunley; Raoul D Nelson; Howard Trachtman; Trevor R P Cole; Maury Pinsk; Detlef Bockenhauer; Mohan Shenoy; Priya Vaidyanathan; John W Foreman; Majid Rasoulpour; Farook Thameem; Hania Z Al-Shahrouri; Jai Radhakrishnan; Ali G Gharavi; Beatrice Goilav; Richard P Lifton
Journal:  Nature       Date:  2012-01-22       Impact factor: 49.962

  6 in total
  13 in total

1.  De novo variants in CUL3 are associated with global developmental delays with or without infantile spasms.

Authors:  Mitsuko Nakashima; Mitsuhiro Kato; Masaru Matsukura; Ryutaro Kira; Lock-Hock Ngu; Klaske D Lichtenbelt; Koen L I van Gassen; Satomi Mitsuhashi; Hirotomo Saitsu; Naomichi Matsumoto
Journal:  J Hum Genet       Date:  2020-04-27       Impact factor: 3.172

2.  Rare cause of severe hypertension in an adolescent boy presenting with short stature: Answers.

Authors:  Zehra Yavas Abali; Gozde Yesil; Tarık Kirkgoz; Neslihan Cicek; Harika Alpay; Serap Turan; Abdullah Bereket; Tulay Guran
Journal:  Pediatr Nephrol       Date:  2019-09-16       Impact factor: 3.714

3.  Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension.

Authors:  Chong Zhang; Nicholas P Meermeier; Andrew S Terker; Katharina I Blankenstein; Jeffrey D Singer; Juliette Hadchouel; David H Ellison; Chao-Ling Yang
Journal:  Biochem Biophys Res Commun       Date:  2015-11-23       Impact factor: 3.575

4.  Novel CUL3 Variant Causing Familial Hyperkalemic Hypertension Impairs Regulation and Function of Ubiquitin Ligase Activity.

Authors:  Harish E Chatrathi; Jason C Collins; Lynne A Wolfe; Thomas C Markello; David R Adams; William A Gahl; Achim Werner; Prashant Sharma
Journal:  Hypertension       Date:  2021-12-02       Impact factor: 10.190

Review 5.  Regulation of with-no-lysine kinase signaling by Kelch-like proteins.

Authors:  Shinichi Uchida; Eisei Sohara; Tatemitsu Rai; Sei Sasaki
Journal:  Biol Cell       Date:  2014-01-10       Impact factor: 4.458

6.  A patient with pseudohypoaldosteronism type II complicated by congenital hypopituitarism carrying a KLHL3 mutation.

Authors:  Marie Mitani; Munehiro Furuichi; Satoshi Narumi; Tomonobu Hasegawa; Motoko Chiga; Shinichi Uchida; Seiji Sato
Journal:  Clin Pediatr Endocrinol       Date:  2016-10-18

7.  Disruption of the with no lysine kinase-STE20-proline alanine-rich kinase pathway reduces the hypertension induced by angiotensin II.

Authors:  Luz G Cervantes-Perez; Maria Castaneda-Bueno; Jose V Jimenez; Norma Vazquez; Lorena Rojas-Vega; Dario R Alessi; Norma A Bobadilla; Gerardo Gamba
Journal:  J Hypertens       Date:  2018-02       Impact factor: 4.844

8.  ROMK expression remains unaltered in a mouse model of familial hyperkalemic hypertension caused by the CUL3Δ403-459 mutation.

Authors:  Meena Murthy; Thimo Kurz; Kevin M O'Shaughnessy
Journal:  Physiol Rep       Date:  2016-07

9.  Evaluation of Phosphorylated Urinary Na-Cl Cotransporter Is Potentially Useful in a Patient With Pseudohypoaldosteronism Type II due to Mutation in CUL3.

Authors:  Keiko Nagahara; Yoshifusa Abe; Akira Hojo; Kazushige Dobashi; Motoko Chiga; Kiyoshi Isobe; Shinichi Uchida; Kazuo Itabashi
Journal:  Glob Pediatr Health       Date:  2014-09-26

10.  Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia.

Authors:  Frances-Rose Schumacher; Keith Siew; Jinwei Zhang; Clare Johnson; Nicola Wood; Sarah E Cleary; Raya S Al Maskari; James T Ferryman; Iris Hardege; Nichola L Figg; Radoslav Enchev; Axel Knebel; Kevin M O'Shaughnessy; Thimo Kurz
Journal:  EMBO Mol Med       Date:  2015-10       Impact factor: 12.137

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