Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology
<p><strong>Background:</strong></p> It is well established that decreased kidney function can increase blood pressure (BP), but it is unproven whether moderately elevated BP causes chronic kidney disease (CKD) or glomerular hyperfiltration. <p><strong>Methods:<...
Main Authors: | , , , , , , , , , , , , , |
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Format: | Journal article |
Language: | English |
Published: |
American Heart Association
2022
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_version_ | 1797109185726382080 |
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author | Staplin, N Herrington, WG Murgia, F Ibrahim, M Bull, KR Judge, P Ng, SYA Turner, M Zhu, D Emberson, J Landray, MJ Baigent, C Haynes, R Hopewell, JC |
author_facet | Staplin, N Herrington, WG Murgia, F Ibrahim, M Bull, KR Judge, P Ng, SYA Turner, M Zhu, D Emberson, J Landray, MJ Baigent, C Haynes, R Hopewell, JC |
author_sort | Staplin, N |
collection | OXFORD |
description | <p><strong>Background:</strong></p>
It is well established that decreased kidney function can increase blood pressure (BP), but it is unproven whether moderately elevated BP causes chronic kidney disease (CKD) or glomerular hyperfiltration.
<p><strong>Methods:</strong></p>
Three hundred eleven thousand one hundred nineteen White British UK Biobank participants were included in logistic regression analyses to estimate the odds of CKD (defined as long-term kidney replacement therapy, estimated glomerular filtration rate [eGFR]<60 mL (min·1.73m2), or urinary albumin:creatinine ratio ≥3 mg/mmol) associated with higher genetically predicted BP using genetic risk scores comprising 219 systolic and 223 diastolic BP loci. Analyses estimating associations with clinical categories of eGFR and urinary albumin:creatinine ratio were also conducted, with an eGFR ≥120 mL (min·1.73m2) considered evidence of glomerular hyperfiltration.
<p><strong>Results:</strong></p>
Twenty-one thousand six hundred twenty-three participants had CKD: 7781 with reduced eGFR and 15 500 with albuminuria. One thousand eight hundred twenty-eight participants had an eGFR ≥120 mL (min·1.73m2). Each genetically predicted 10 mm Hg higher systolic BP and 5 mm Hg higher diastolic BP were associated with a 37% (95% CI, 1.29–1.45) and 19% (1.14–1.25) higher odds of CKD, respectively. Associations were evident for both the reduced eGFR and albuminuria components of the CKD outcome. The odds of hyperfiltration (versus an eGFR ≥60 and <90 mL[min·1.73m2]) were 49% higher (95% CI, 1.21–1.84) for each genetically predicted 10 mm Hg higher systolic BP. Associations with CKD and hyperfiltration were similar irrespective of preexisting diabetes, vascular disease, or different levels of adiposity.
<p><strong>Conclusions:</strong></p>
In this general population, genetic epidemiological evidence supports a causal role of life-long differences in BP for decreased kidney function, glomerular hyperfiltration, and albuminuria. Physiological autoregulation may not afford complete renal protection against the moderate BP elevations. |
first_indexed | 2024-03-07T07:38:23Z |
format | Journal article |
id | oxford-uuid:aefe90da-8a81-4cfa-981a-bb36eca6faa3 |
institution | University of Oxford |
language | English |
last_indexed | 2024-03-07T07:38:23Z |
publishDate | 2022 |
publisher | American Heart Association |
record_format | dspace |
spelling | oxford-uuid:aefe90da-8a81-4cfa-981a-bb36eca6faa32023-03-27T11:26:54ZDetermining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiologyJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:aefe90da-8a81-4cfa-981a-bb36eca6faa3EnglishSymplectic ElementsAmerican Heart Association2022Staplin, NHerrington, WGMurgia, FIbrahim, MBull, KRJudge, PNg, SYATurner, MZhu, DEmberson, JLandray, MJBaigent, CHaynes, RHopewell, JC<p><strong>Background:</strong></p> It is well established that decreased kidney function can increase blood pressure (BP), but it is unproven whether moderately elevated BP causes chronic kidney disease (CKD) or glomerular hyperfiltration. <p><strong>Methods:</strong></p> Three hundred eleven thousand one hundred nineteen White British UK Biobank participants were included in logistic regression analyses to estimate the odds of CKD (defined as long-term kidney replacement therapy, estimated glomerular filtration rate [eGFR]<60 mL (min·1.73m2), or urinary albumin:creatinine ratio ≥3 mg/mmol) associated with higher genetically predicted BP using genetic risk scores comprising 219 systolic and 223 diastolic BP loci. Analyses estimating associations with clinical categories of eGFR and urinary albumin:creatinine ratio were also conducted, with an eGFR ≥120 mL (min·1.73m2) considered evidence of glomerular hyperfiltration. <p><strong>Results:</strong></p> Twenty-one thousand six hundred twenty-three participants had CKD: 7781 with reduced eGFR and 15 500 with albuminuria. One thousand eight hundred twenty-eight participants had an eGFR ≥120 mL (min·1.73m2). Each genetically predicted 10 mm Hg higher systolic BP and 5 mm Hg higher diastolic BP were associated with a 37% (95% CI, 1.29–1.45) and 19% (1.14–1.25) higher odds of CKD, respectively. Associations were evident for both the reduced eGFR and albuminuria components of the CKD outcome. The odds of hyperfiltration (versus an eGFR ≥60 and <90 mL[min·1.73m2]) were 49% higher (95% CI, 1.21–1.84) for each genetically predicted 10 mm Hg higher systolic BP. Associations with CKD and hyperfiltration were similar irrespective of preexisting diabetes, vascular disease, or different levels of adiposity. <p><strong>Conclusions:</strong></p> In this general population, genetic epidemiological evidence supports a causal role of life-long differences in BP for decreased kidney function, glomerular hyperfiltration, and albuminuria. Physiological autoregulation may not afford complete renal protection against the moderate BP elevations. |
spellingShingle | Staplin, N Herrington, WG Murgia, F Ibrahim, M Bull, KR Judge, P Ng, SYA Turner, M Zhu, D Emberson, J Landray, MJ Baigent, C Haynes, R Hopewell, JC Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title | Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title_full | Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title_fullStr | Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title_full_unstemmed | Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title_short | Determining the relationship between blood pressure, kidney function, and chronic kidney disease: insights from genetic epidemiology |
title_sort | determining the relationship between blood pressure kidney function and chronic kidney disease insights from genetic epidemiology |
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