Literature DB >> 31558682

Identification of Acer2 as a First Susceptibility Gene for Lithium-Induced Nephrogenic Diabetes Insipidus in Mice.

Theun de Groot1,2,3, Lena K Ebert1,2,4, Birgitte Mønster Christensen5, Karolina Andralojc6,7,8, Lydie Cheval9,10, Alain Doucet9, Cungui Mao11,12, Ruben Baumgarten13, Benjamin E Low1, Roger Sandhoff14,15, Michael V Wiles1, Peter M T Deen16, Ron Korstanje17.   

Abstract

BACKGROUND: Lithium, mainstay treatment for bipolar disorder, causes nephrogenic diabetes insipidus and hypercalcemia in about 20% and 10% of patients, respectively, and may lead to acidosis. These adverse effects develop in only a subset of patients treated with lithium, suggesting genetic factors play a role.
METHODS: To identify susceptibility genes for lithium-induced adverse effects, we performed a genome-wide association study in mice, which develop such effects faster than humans. On day 8 and 10 after assigning female mice from 29 different inbred strains to normal chow or lithium diet (40 mmol/kg), we housed the animals for 48 hours in metabolic cages for urine collection. We also collected blood samples.
RESULTS: In 17 strains, lithium treatment significantly elevated urine production, whereas the other 12 strains were not affected. Increased urine production strongly correlated with lower urine osmolality and elevated water intake. Lithium caused acidosis only in one mouse strain, whereas hypercalcemia was found in four strains. Lithium effects on blood pH or ionized calcium did not correlate with effects on urine production. Using genome-wide association analyses, we identified eight gene-containing loci, including a locus containing Acer2, which encodes a ceramidase and is specifically expressed in the collecting duct. Knockout of Acer2 led to increased susceptibility for lithium-induced diabetes insipidus development.
CONCLUSIONS: We demonstrate that genome-wide association studies in mice can be used successfully to identify susceptibility genes for development of lithium-induced adverse effects. We identified Acer2 as a first susceptibility gene for lithium-induced diabetes insipidus in mice.
Copyright © 2019 by the American Society of Nephrology.

Entities:  

Keywords:  acidosis; calcium; genetics and development; water-electrolyte balance

Mesh:

Substances:

Year:  2019        PMID: 31558682      PMCID: PMC6900794          DOI: 10.1681/ASN.2018050549

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  53 in total

1.  Revisiting lithium-associated hyperparathyroidism in the era of intraoperative parathyroid hormone monitoring.

Authors:  Jonathan C Hundley; Derek T Woodrum; Brian D Saunders; Gerard M Doherty; Paul G Gauger
Journal:  Surgery       Date:  2005-12       Impact factor: 3.982

2.  Renal sulfatides: sphingoid base-dependent localization and region-specific compensation of CerS2-dysfunction.

Authors:  Christian Marsching; Mariona Rabionet; Daniel Mathow; Richard Jennemann; Christiane Kremser; Stefan Porubsky; Christian Bolenz; Klaus Willecke; Hermann-Josef Gröne; Carsten Hopf; Roger Sandhoff
Journal:  J Lipid Res       Date:  2014-09-29       Impact factor: 5.922

3.  alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus.

Authors:  Birgitte Mønster Christensen; Annie Mercier Zuber; Johannes Loffing; Jean-Christophe Stehle; Peter M T Deen; Bernard C Rossier; Edith Hummler
Journal:  J Am Soc Nephrol       Date:  2010-11-04       Impact factor: 10.121

4.  Lithium-induced impairment of urine acidification.

Authors:  J M Roscoe; M B Goldstein; M L Halperin; D R Wilson; B J Stinebaugh
Journal:  Kidney Int       Date:  1976-04       Impact factor: 10.612

5.  Lithium-induced nephrogenic diabetes insipidus.

Authors:  K A Stone
Journal:  J Am Board Fam Pract       Date:  1999 Jan-Feb

6.  Evaluation of Polyuria: The Roles of Solute Loading and Water Diuresis.

Authors:  Bhavna Bhasin; Juan Carlos Q Velez
Journal:  Am J Kidney Dis       Date:  2015-12-11       Impact factor: 8.860

Review 7.  Risk of recurrence following discontinuation of lithium treatment in bipolar disorder.

Authors:  T Suppes; R J Baldessarini; G L Faedda; M Tohen
Journal:  Arch Gen Psychiatry       Date:  1991-12

8.  The tyrosine phosphatase PTPRD is a tumor suppressor that is frequently inactivated and mutated in glioblastoma and other human cancers.

Authors:  Selvaraju Veeriah; Cameron Brennan; Shasha Meng; Bhuvanesh Singh; James A Fagin; David B Solit; Philip B Paty; Dan Rohle; Igor Vivanco; Juliann Chmielecki; William Pao; Marc Ladanyi; William L Gerald; Linda Liau; Timothy C Cloughesy; Paul S Mischel; Chris Sander; Barry Taylor; Nikolaus Schultz; John Major; Adriana Heguy; Fang Fang; Ingo K Mellinghoff; Timothy A Chan
Journal:  Proc Natl Acad Sci U S A       Date:  2009-05-28       Impact factor: 11.205

9.  Effects of chronic lithium administration on renal acid excretion in humans and rats.

Authors:  I David Weiner; John P Leader; Jennifer J Bedford; Jill W Verlander; Gaye Ellis; Priyakshi Kalita; Frederiek Vos; Sylvia de Jong; Robert J Walker
Journal:  Physiol Rep       Date:  2014-12-11

10.  The Ensembl Variant Effect Predictor.

Authors:  William McLaren; Laurent Gil; Sarah E Hunt; Harpreet Singh Riat; Graham R S Ritchie; Anja Thormann; Paul Flicek; Fiona Cunningham
Journal:  Genome Biol       Date:  2016-06-06       Impact factor: 13.583

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  2 in total

Review 1.  Using Genetic and Species Diversity to Tackle Kidney Disease.

Authors:  Michael R Garrett; Ron Korstanje
Journal:  Trends Genet       Date:  2020-04-30       Impact factor: 11.639

Review 2.  The impact of genetic background on mouse models of kidney disease.

Authors:  Rei Bufi; Ron Korstanje
Journal:  Kidney Int       Date:  2022-04-13       Impact factor: 18.998

  2 in total

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