Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53
Aboriginal Australians are at high risk of cardiovascular, metabolic and renal diseases, resulting in a marked reduction in life expectancy when compared to the rest of the Australian population. This is partly due to recognized environmental and lifestyle risk factors, but a contribution of genetic...
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description | Aboriginal Australians are at high risk of cardiovascular, metabolic and renal diseases, resulting in a marked reduction in life expectancy when compared to the rest of the Australian population. This is partly due to recognized environmental and lifestyle risk factors, but a contribution of genetic susceptibility is also likely.
Using results from a comprehensive survey of one community (N = 1350 examined individuals), we have tested for familial aggregation of plasma glucose, arterial blood pressure, albuminuria (measured as urinary albumin to creatinine ratio, UACR) and estimated glomerular filtration rate (eGFR), and quantified the contribution of variation at four candidate genes (ACE; TP53; ENOS3; MTHFR).
In the subsample of 357 individuals with complete genotype and phenotype data we showed that both UACR (h
= 64%) and blood pressure (sBP h
= 29%, dBP, h
= 11%) were significantly heritable. The ACE insertion-deletion (P = 0.0009) and TP53 codon72 polymorphisms (P = 0.003) together contributed approximately 15% of the total heritability of UACR, with an effect of ACE genotype on BP also clearly evident.
While the effects of the ACE insertion-deletion on risk of renal disease (especially in the setting of diabetes) are well recognized, this is only the second study to implicate p53 genotype as a risk factor for albuminuria - the other being an earlier study we performed in a different Aboriginal community (McDonald et al., J Am Soc Nephrol 13: 677-83, 2002). We conclude that there are significant genetic contributions to the high prevalence of chronic diseases observed in this population. |
doi_str_mv | 10.1186/s12882-016-0396-2 |
format | Article |
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Using results from a comprehensive survey of one community (N = 1350 examined individuals), we have tested for familial aggregation of plasma glucose, arterial blood pressure, albuminuria (measured as urinary albumin to creatinine ratio, UACR) and estimated glomerular filtration rate (eGFR), and quantified the contribution of variation at four candidate genes (ACE; TP53; ENOS3; MTHFR).
In the subsample of 357 individuals with complete genotype and phenotype data we showed that both UACR (h
= 64%) and blood pressure (sBP h
= 29%, dBP, h
= 11%) were significantly heritable. The ACE insertion-deletion (P = 0.0009) and TP53 codon72 polymorphisms (P = 0.003) together contributed approximately 15% of the total heritability of UACR, with an effect of ACE genotype on BP also clearly evident.
While the effects of the ACE insertion-deletion on risk of renal disease (especially in the setting of diabetes) are well recognized, this is only the second study to implicate p53 genotype as a risk factor for albuminuria - the other being an earlier study we performed in a different Aboriginal community (McDonald et al., J Am Soc Nephrol 13: 677-83, 2002). We conclude that there are significant genetic contributions to the high prevalence of chronic diseases observed in this population.</description><identifier>ISSN: 1471-2369</identifier><identifier>EISSN: 1471-2369</identifier><identifier>DOI: 10.1186/s12882-016-0396-2</identifier><identifier>PMID: 27871254</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Albuminuria ; Albuminuria - genetics ; Albuminuria - urine ; Arterial Pressure - genetics ; Australian aborigines ; Blood Glucose - genetics ; Creatinine - urine ; Female ; Genes, p53 ; Genetic aspects ; Genetic variation ; Genotype ; Glomerular Filtration Rate - genetics ; Health aspects ; Humans ; Hypertension - genetics ; INDEL Mutation ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) - genetics ; Middle Aged ; Nephrology ; Nitric Oxide Synthase Type III - genetics ; Pedigree ; Peptidyl-Dipeptidase A - genetics ; Phenotype ; Physiological aspects ; Polymorphism, Genetic ; Pulmonary hypertension ; Risk factors ; Surveys ; Young Adult</subject><ispartof>BMC nephrology, 2016-11, Vol.17 (1), p.183, Article 183</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-82dfb5ea7d8337669b91288c38f37fea21197fbfc7aac3b21e336e1cf829d9833</citedby><cites>FETCH-LOGICAL-c520t-82dfb5ea7d8337669b91288c38f37fea21197fbfc7aac3b21e336e1cf829d9833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117595/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117595/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27871254$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Duffy, David L</creatorcontrib><creatorcontrib>McDonald, Stephen P</creatorcontrib><creatorcontrib>Hayhurst, Beverley</creatorcontrib><creatorcontrib>Panagiotopoulos, Sianna</creatorcontrib><creatorcontrib>Smith, Trudy J</creatorcontrib><creatorcontrib>Wang, Xing L</creatorcontrib><creatorcontrib>Wilcken, David E</creatorcontrib><creatorcontrib>Duarte, Natalia L</creatorcontrib><creatorcontrib>Mathews, John</creatorcontrib><creatorcontrib>Hoy, Wendy E</creatorcontrib><title>Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53</title><title>BMC nephrology</title><addtitle>BMC Nephrol</addtitle><description>Aboriginal Australians are at high risk of cardiovascular, metabolic and renal diseases, resulting in a marked reduction in life expectancy when compared to the rest of the Australian population. This is partly due to recognized environmental and lifestyle risk factors, but a contribution of genetic susceptibility is also likely.
Using results from a comprehensive survey of one community (N = 1350 examined individuals), we have tested for familial aggregation of plasma glucose, arterial blood pressure, albuminuria (measured as urinary albumin to creatinine ratio, UACR) and estimated glomerular filtration rate (eGFR), and quantified the contribution of variation at four candidate genes (ACE; TP53; ENOS3; MTHFR).
In the subsample of 357 individuals with complete genotype and phenotype data we showed that both UACR (h
= 64%) and blood pressure (sBP h
= 29%, dBP, h
= 11%) were significantly heritable. The ACE insertion-deletion (P = 0.0009) and TP53 codon72 polymorphisms (P = 0.003) together contributed approximately 15% of the total heritability of UACR, with an effect of ACE genotype on BP also clearly evident.
While the effects of the ACE insertion-deletion on risk of renal disease (especially in the setting of diabetes) are well recognized, this is only the second study to implicate p53 genotype as a risk factor for albuminuria - the other being an earlier study we performed in a different Aboriginal community (McDonald et al., J Am Soc Nephrol 13: 677-83, 2002). We conclude that there are significant genetic contributions to the high prevalence of chronic diseases observed in this population.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Albuminuria</subject><subject>Albuminuria - genetics</subject><subject>Albuminuria - urine</subject><subject>Arterial Pressure - genetics</subject><subject>Australian aborigines</subject><subject>Blood Glucose - genetics</subject><subject>Creatinine - urine</subject><subject>Female</subject><subject>Genes, p53</subject><subject>Genetic aspects</subject><subject>Genetic variation</subject><subject>Genotype</subject><subject>Glomerular Filtration Rate - genetics</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hypertension - genetics</subject><subject>INDEL Mutation</subject><subject>Male</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</subject><subject>Middle Aged</subject><subject>Nephrology</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Pedigree</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Polymorphism, Genetic</subject><subject>Pulmonary hypertension</subject><subject>Risk factors</subject><subject>Surveys</subject><subject>Young Adult</subject><issn>1471-2369</issn><issn>1471-2369</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptksFu3CAURa2qUZMm_YBuKkvddOOUB2MDm0rWKGkrRWoWyRphDB4iG6ZgR5r_yAcXZpI0qSokg3jnXvDjFsVHQOcArPkaATOGKwRNhQhvKvymOIEVhQqThr99sT4u3sd4hxBQtkLvimNMGQVcr06Kh0s52dHKsZTDEPQgZ-td6U0px26ZrFuClaV0fSnDrEPmNrutTmsXM2hdKpZt54MdrEvVdolzkMnQlcpP0-LsvNvr541OO24OtluezriXydHNMdu064s9d3Ndk7PiyMgx6g-P82lxe3lxs_5RXf36_nPdXlWqxmiuGO5NV2tJe0YIbRre8dwQRZgh1GiJATg1nVFUSkU6DJqQRoMyDPOeJ81p8e3gu126SfdKu3x3sQ12kmEnvLTidcXZjRj8vagBaM3rZPDl0SD434uOs5hsVHocpdN-iQLYCjcofxP6-R_0zi8htWxP1QQIx-gvNchRC-uMT-eqbCra9JjpARvGE3X-HyqNXk82NVkbm_ZfCeAgUMHHGLR5_kdAIkdJHKIkUpREjpLIF_70sjnPiqfskD8lEMWo</recordid><startdate>20161121</startdate><enddate>20161121</enddate><creator>Duffy, David L</creator><creator>McDonald, Stephen P</creator><creator>Hayhurst, Beverley</creator><creator>Panagiotopoulos, Sianna</creator><creator>Smith, Trudy J</creator><creator>Wang, Xing L</creator><creator>Wilcken, David E</creator><creator>Duarte, Natalia L</creator><creator>Mathews, John</creator><creator>Hoy, Wendy E</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161121</creationdate><title>Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53</title><author>Duffy, David L ; 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This is partly due to recognized environmental and lifestyle risk factors, but a contribution of genetic susceptibility is also likely.
Using results from a comprehensive survey of one community (N = 1350 examined individuals), we have tested for familial aggregation of plasma glucose, arterial blood pressure, albuminuria (measured as urinary albumin to creatinine ratio, UACR) and estimated glomerular filtration rate (eGFR), and quantified the contribution of variation at four candidate genes (ACE; TP53; ENOS3; MTHFR).
In the subsample of 357 individuals with complete genotype and phenotype data we showed that both UACR (h
= 64%) and blood pressure (sBP h
= 29%, dBP, h
= 11%) were significantly heritable. The ACE insertion-deletion (P = 0.0009) and TP53 codon72 polymorphisms (P = 0.003) together contributed approximately 15% of the total heritability of UACR, with an effect of ACE genotype on BP also clearly evident.
While the effects of the ACE insertion-deletion on risk of renal disease (especially in the setting of diabetes) are well recognized, this is only the second study to implicate p53 genotype as a risk factor for albuminuria - the other being an earlier study we performed in a different Aboriginal community (McDonald et al., J Am Soc Nephrol 13: 677-83, 2002). We conclude that there are significant genetic contributions to the high prevalence of chronic diseases observed in this population.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>27871254</pmid><doi>10.1186/s12882-016-0396-2</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Albuminuria Albuminuria - genetics Albuminuria - urine Arterial Pressure - genetics Australian aborigines Blood Glucose - genetics Creatinine - urine Female Genes, p53 Genetic aspects Genetic variation Genotype Glomerular Filtration Rate - genetics Health aspects Humans Hypertension - genetics INDEL Mutation Male Methylenetetrahydrofolate Reductase (NADPH2) - genetics Middle Aged Nephrology Nitric Oxide Synthase Type III - genetics Pedigree Peptidyl-Dipeptidase A - genetics Phenotype Physiological aspects Polymorphism, Genetic Pulmonary hypertension Risk factors Surveys Young Adult |
title | Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53 |
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