Recurrent FXYD2 p.Gly41Arg mutation in patients with isolated dominant hypomagnesaemia

Jeroen H. F. de Baaij, Eiske M. Dorresteijn, Eric A. M. Hennekam, Erik-Jan Kamsteeg, Rowdy Meijer, Karin Dahan, Michelle Muller, Marinus A. van den Dorpel, Rene J. M. Bindels, Joost G. J. Hoenderop, Olivier Devuyst, Nine V. A. M. Knoers*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background. Magnesium (Mg2+) is an essential ion for cell growth, neuroplasticity and muscle contraction. Blood Mg2+ levels

Methods. Here, two families with hypomagnesaemia and hypocalciuria were screened for mutations in the FXYD2 gene. Moreover, the patients were clinically and genetically characterized.

Results. We report a p.Gly41Arg FXYD2 mutation in two families with hypomagnesaemia and hypocalciuria. Interestingly, this is the same mutation as was described in the original study. As in the initial family, several patients suffered from muscle cramps, chondrocalcinosis and epilepsy. Haplotype analysis revealed an overlapping haplotype in all families, suggesting a founder effect.

Conclusions. The recurrent p.Gly41Arg FXYD2 mutation in two new families with IDH confirms that FXYD2 mutation causes hypomagnesaemia. Until now, no other FXYD2 mutations have been reported which could indicate that other FXYD2 mutations will not cause hypomagnesaemia or are embryonically lethal.

Original languageEnglish
Pages (from-to)952-957
Number of pages6
JournalNephrology Dialysis Transplantation
Volume30
Issue number6
DOIs
Publication statusPublished - Jun 2015

Keywords

  • distal convoluted tubule
  • FXYD2
  • kidney
  • magnesium
  • Na+-K+-ATPase
  • RENAL MAGNESIUM LOSS
  • NA+,K+-ATPASE GAMMA-SUBUNIT
  • RAT-KIDNEY
  • HYPOKALEMIA

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