Autosomal dominant neurohypophyseal diabetes insipidus with linkage to chromosome 20p13 but without mutations in the AVP-NPII gene

J Clin Endocrinol Metab. 2005 Jul;90(7):4388-93. doi: 10.1210/jc.2004-2000. Epub 2005 Apr 5.

Abstract

Context: Autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) has been known as a rare disorder transmitted as an autosomal dominant trait, characterized by polyuria and polydipsia, and caused by deficient neurosecretion of arginine vasopressin precursor (AVP-NPII). We reported an ADNDI family with linkage to chromosome 20p13 but without mutations in the AVP-NPII gene.

Objective: The objective of this study was to identify the corresponding locus responsible for ADNDI in a family without AVP-NP II gene mutations.

Subjects and methods: Two families with ADNDI were diagnosed by water deprivation test. The AVP-NPII gene was amplified by PCR and sequenced. A genomewide scan was performed in one family using 400 microsatellite markers covering 22 autosomes.

Results: A 3-bp deletion (1827-1829delAGG) of AVP-NPII gene was identified in the affected individuals in one family. Although no mutations could be detected in the coding, the promoter, and intronic regions of AVP-NPII gene in the other family, a maximum LOD score of 1.202999 (theta = 0.00) was obtained at marker D20S889 by genomewide scan, and a 7-cM interval on chromosome 20p13 was defined by fine mapping with markers D20S199-D20S849. Furthermore, the intragenic region that regulates AVP-NPII and oxytocin expression as an enhancer element and the UBCE7IP5 gene that participates in prohormone degradation were sequenced. No alterations could be detected either.

Conclusion: The corresponding locus responsible for ADNDI is possibly heterogeneous regarding the slightly different clinical features in these two families.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Chromosomes, Human, Pair 20*
  • Diabetes Insipidus, Neurogenic / genetics*
  • Genes, Dominant*
  • Genetic Linkage*
  • Haplotypes
  • Humans
  • Male
  • Middle Aged
  • Mutation*
  • Neurophysins / genetics*
  • Polymerase Chain Reaction
  • Protein Precursors / genetics*
  • Vasopressins / genetics*

Substances

  • AVP protein, human
  • Neurophysins
  • Protein Precursors
  • Vasopressins