| Progression of chronic kidney disease: Adrenergic genetic influence on glomerular filtration rate decline in hypertensive nephrosclerosis. | |
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MedLine Citation:
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PMID: 20484896 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: African-Americans are likely to develop hypertension and hypertensive nephrosclerosis. This grave prognosis, coupled with familial aggregation of end-stage renal disease (ESRD) in Blacks, prompts a search for genetic risk factors for ESRD. Recent evidence implicates a crucial role for the sympathetic nervous system in progressive renal disease. METHODS: We used the African-American Study of Kidney Disease to probe whether beta2-adrenergic receptor (ADRB2) predicts glomerular filtration rate (GFR) decline rate. A total of 580 participants were included. Baseline GFR was 51.2 +/- 0.5 ml/min/1.73 m2. Subjects were randomized in a 2 x 3 block design: to intensively lowered (MAP < or = 92 mm Hg) versus 'usual' (MAP = 102-107 mm Hg) blood pressure goal groups, and also divided by three randomized antihypertensive drugs (ramipril, metoprolol, or amlodipine). We scored 4 SNPs at the ADRB2 locus. RESULTS: Haplotypes at ADRB2 predicted chronic GFR decline rate, GFR declined more slowly in individuals with haplotype-1 (-804G-->173T-->16Gly-->27GIn), and faster in those who carried haplotype-3 (-804G-->173T-->16Arg-->27Gln). ADRB2 genotype interacted with antihypertensive drug class to influence GFR slope (p = 0.001-0.037). We extended our findings to an independent case/control sample of Black hypertensive ESRD, in which we found that variant Gly16Arg that tagged the GFR slope-determining ADRB2 haplotype also conferred risk for the ESRD trait in Blacks. CONCLUSIONS: The GFR decline/progression rate in hypertensive renal disease is controlled in part by genetic variation within the adrenergic pathway. |
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Authors:
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Yuqing Chen; Michael S Lipkowitz; Rany M Salem; Maple M Fung; Vibha Bhatnagar; Manjula Mahata; Caroline M Nievergelt; Fangwen Rao; Sushil K Mahata; Nicholas J Schork; Pamela J Hicks; Donald W Bowden; Barry I Freedman; Victoria H Brophy; Daniel T O'Connor; |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2010-05-19 |
Journal Detail:
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Title: American journal of nephrology Volume: 32 ISSN: 1421-9670 ISO Abbreviation: Am. J. Nephrol. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-07-19 Completed Date: 2010-10-25 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 8109361 Medline TA: Am J Nephrol Country: Switzerland |
Other Details:
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Languages: eng Pagination: 23-30 Citation Subset: IM |
Copyright Information:
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Copyright 2010 S. Karger AG, Basel. |
Affiliation:
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Renal Division, Peking University First Hospital, Beijing, China. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult African Americans / genetics* Aged Antihypertensive Agents / therapeutic use* Disease Progression Drug Resistance / genetics Female Glomerular Filtration Rate / drug effects, genetics Humans Hypertension, Renal* / drug therapy, ethnology, genetics Male Middle Aged Multicenter Studies as Topic Nephrosclerosis* / drug therapy, ethnology, genetics Randomized Controlled Trials as Topic Receptors, Adrenergic, beta-2 / genetics* Renal Insufficiency, Chronic* / drug therapy, ethnology, genetics Young Adult |
| Grant Support | |
ID/Acronym/Agency:
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M01 RR000827-346233/RR/NCRR NIH HHS; MD000220/MD/NCMHD NIH HHS; RR00827/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Receptors, Adrenergic, beta-2 |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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