{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:36:49Z","timestamp":1745469409944,"version":"3.40.4"},"reference-count":39,"publisher":"S. Karger AG","issue":"1","license":[{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am J Nephrol"],"published-print":{"date-parts":[[2010]]},"abstract":"<jats:p>&lt;i&gt;Background:&lt;\/i&gt; 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. &lt;i&gt;Methods:&lt;\/i&gt; We used the African-American Study of Kidney Disease to probe whether \u03b2&lt;sub&gt;2&lt;\/sub&gt;-adrenergic receptor (&lt;i&gt;ADRB2)&lt;\/i&gt; predicts glomerular filtration rate (GFR) decline rate. A total of 580 participants were included. Baseline GFR was 51.2 \u00b1 0.5 ml\/min\/1.73 m&lt;sup&gt;2&lt;\/sup&gt;. Subjects were randomized in a 2 \u00d7 3 block design: to intensively lowered (MAP \u226492 mm Hg) versus \u2018usual\u2019 (MAP = 102\u2013107 mm Hg) blood pressure goal groups, and also divided by three randomized antihypertensive drugs (ramipril, metoprolol, or amlodipine). We scored 4 SNPs at the &lt;i&gt;ADRB2&lt;\/i&gt; locus. &lt;i&gt;Results:&lt;\/i&gt; Haplotypes at &lt;i&gt;ADRB2&lt;\/i&gt; predicted chronic GFR decline rate, GFR declined more slowely in individuals with haplotype-1 (\u2013804G\u2192173T\u219216Gly\u219227GIn), and faster in those who carried haplotype-3 (\u2013804G\u2192173T\u219216Arg\u219227Gln). &lt;i&gt;ADRB2&lt;\/i&gt; genotype interacted with antihypertensive drug class to influence GFR slope (p = 0.001\u20130.037). 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 &lt;i&gt;ADRB2&lt;\/i&gt; haplotype also conferred risk for the ESRD trait in Blacks. &lt;i&gt;Conclusions:&lt;\/i&gt; The GFR decline\/progression rate in hypertensive renal disease is controlled in part by genetic variation within the adrenergic pathway.<\/jats:p>","DOI":"10.1159\/000313927","type":"journal-article","created":{"date-parts":[[2010,5,19]],"date-time":"2010-05-19T07:38:48Z","timestamp":1274254728000},"page":"23-30","source":"Crossref","is-referenced-by-count":11,"title":["Progression of Chronic Kidney Disease: Adrenergic Genetic Influence on Glomerular Filtration Rate Decline in Hypertensive Nephrosclerosis"],"prefix":"10.1159","volume":"32","author":[{"given":"Yuqing","family":"Chen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael 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