Genetic variants of calcium and vitamin D metabolism in kidney stone disease
Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephro...
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| Vydáno v: | Nature communications Ročník 10; číslo 1; s. 5175 - 10 |
|---|---|
| Hlavní autoři: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
15.11.2019
Nature Publishing Group Nature Portfolio |
| Témata: | |
| ISSN: | 2041-1723, 2041-1723 |
| On-line přístup: | Získat plný text |
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| Abstract | Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A
CYP24A1
locus is predicted to affect vitamin D metabolism and five loci,
DGKD, DGKH, WDR72, GPIC1
, and
BCR
, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the
CYP24A1-
associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the
DGKD-
associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted.
Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca
2+
and oxalate. Here, the authors report genome-wide association analyses for kidney stone disease, report seven previously unknown loci and find that some of these loci also associate with Ca
2+
concentration and excretion. |
|---|---|
| AbstractList | Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted.Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca2+ and oxalate. Here, the authors report genome-wide association analyses for kidney stone disease, report seven previously unknown loci and find that some of these loci also associate with Ca2+ concentration and excretion. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1 , and BCR , are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1- associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD- associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca 2+ and oxalate. Here, the authors report genome-wide association analyses for kidney stone disease, report seven previously unknown loci and find that some of these loci also associate with Ca 2+ concentration and excretion. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45-60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted.Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45-60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca2+ and oxalate. Here, the authors report genome-wide association analyses for kidney stone disease, report seven previously unknown loci and find that some of these loci also associate with Ca2+ concentration and excretion. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1 , and BCR , are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1- associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD- associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45-60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted. Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca2+ and oxalate. Here, the authors report genome-wide association analyses for kidney stone disease, report seven previously unknown loci and find that some of these loci also associate with Ca2+ concentration and excretion. |
| ArticleNumber | 5175 |
| Author | Wiberg, Akira Thakker, Rajesh V. Grout, Emily Terao, Chikashi Ng, Michael Kamatani, Yoichiro Matsuda, Koichi Tanikawa, Chizu Turney, Benjamin W. Furniss, Dominic Howles, Sarah A. Takahashi, Atsushi Kubo, Michiaki Goldsworthy, Michelle Gluck, Anna K. Bayliss, Asha L. |
| Author_xml | – sequence: 1 givenname: Sarah A. orcidid: 0000-0001-6342-0895 surname: Howles fullname: Howles, Sarah A. email: sarah.howles@nds.ox.ac.uk organization: Nuffield Department of Surgical Sciences, University of Oxford, Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford – sequence: 2 givenname: Akira orcidid: 0000-0003-4944-123X surname: Wiberg fullname: Wiberg, Akira organization: Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford – sequence: 3 givenname: Michelle orcidid: 0000-0003-1354-7737 surname: Goldsworthy fullname: Goldsworthy, Michelle organization: Nuffield Department of Surgical Sciences, University of Oxford, Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford – sequence: 4 givenname: Asha L. surname: Bayliss fullname: Bayliss, Asha L. organization: Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford – sequence: 5 givenname: Anna K. orcidid: 0000-0003-3459-2764 surname: Gluck fullname: Gluck, Anna K. organization: Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford – sequence: 6 givenname: Michael orcidid: 0000-0003-3463-5568 surname: Ng fullname: Ng, Michael organization: Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford – sequence: 7 givenname: Emily surname: Grout fullname: Grout, Emily organization: Nuffield Department of Surgical Sciences, University of Oxford – sequence: 8 givenname: Chizu surname: Tanikawa fullname: Tanikawa, Chizu organization: Laboratory of Genome Technology, Human Genome Centre, University of Tokyo – sequence: 9 givenname: Yoichiro orcidid: 0000-0001-8748-5597 surname: Kamatani fullname: Kamatani, Yoichiro organization: RIKEN Centre for Integrative Medical Sciences – sequence: 10 givenname: Chikashi orcidid: 0000-0002-6452-4095 surname: Terao fullname: Terao, Chikashi organization: RIKEN Centre for Integrative Medical Sciences – sequence: 11 givenname: Atsushi orcidid: 0000-0001-7099-8767 surname: Takahashi fullname: Takahashi, Atsushi organization: RIKEN Centre for Integrative Medical Sciences – sequence: 12 givenname: Michiaki surname: Kubo fullname: Kubo, Michiaki organization: RIKEN Centre for Integrative Medical Sciences – sequence: 13 givenname: Koichi orcidid: 0000-0001-7292-2686 surname: Matsuda fullname: Matsuda, Koichi organization: Laboratory of Clinical Genome Sequencing, Department of Computational Biology and Medical Sciences, University of Tokyo – sequence: 14 givenname: Rajesh V. orcidid: 0000-0002-1438-3220 surname: Thakker fullname: Thakker, Rajesh V. organization: Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford – sequence: 15 givenname: Benjamin W. surname: Turney fullname: Turney, Benjamin W. organization: Nuffield Department of Surgical Sciences, University of Oxford – sequence: 16 givenname: Dominic orcidid: 0000-0003-2780-7173 surname: Furniss fullname: Furniss, Dominic organization: Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31729369$$D View this record in MEDLINE/PubMed |
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| Copyright | The Author(s) 2019. corrected publication 2022 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Author(s) 2019. corrected publication 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Author(s) 2019, corrected publication 2022 |
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| DOI | 10.1038/s41467-019-13145-x |
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| Snippet | Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association... Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45-60%. We present genome-wide association... Kidney stones form in the presence of overabundance of crystal-forming substances such as Ca2+ and oxalate. Here, the authors report genome-wide association... |
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| SubjectTerms | 13/95 45 631/208/205/2138 631/443/810 631/80/86/1999 692/4022/1585/273 Adult Aged Asian People - genetics Calciferol Calcium Calcium (blood) Calcium (urinary) Calcium - metabolism Calcium ions Calcium oxalate Calcium signalling Calcium-sensing receptors Calculi Diacylglycerol Kinase - genetics Diacylglycerol Kinase - metabolism Dietary supplements Excretion Female Genetic diversity Genetic variance Genetic Variation Genome-wide association studies Genome-Wide Association Study Genomes Genotype Genotypes Heritability Humanities and Social Sciences Humans Japan Kidney Calculi - genetics Kidney Calculi - metabolism Kidney stones Kidneys Loci Male Metabolism Middle Aged multidisciplinary Nephrolithiasis Oxalic acid Patients Polymorphism, Single Nucleotide Precision medicine Prospective Studies Proteins - genetics Proteins - metabolism Receptors, Calcium-Sensing - genetics Receptors, Calcium-Sensing - metabolism Science Signal transduction Signaling Supplements United Kingdom Vitamin D Vitamin D - metabolism White People - genetics |
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| Title | Genetic variants of calcium and vitamin D metabolism in kidney stone disease |
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