Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study

Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Natalia Campos‐Obando [verfasserIn] Ariadne Bosman [verfasserIn] Maryam Kavousi [verfasserIn] Carolina Medina‐Gomez [verfasserIn] Bram C. J. van der Eerden [verfasserIn] Daniel Bos [verfasserIn] Oscar H. Franco [verfasserIn] André G. Uitterlinden [verfasserIn] M. Carola Zillikens [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate

Übergeordnetes Werk:	In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease - Wiley, 2012, 11(2022), 15
Übergeordnetes Werk:	volume:11 ; year:2022 ; number:15

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1161/JAHA.121.023024

Katalog-ID:	DOAJ081326386

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100	0		\|a Natalia Campos‐Obando \|e verfasserin \|4 aut
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520			\|a Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed.
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allfields	10.1161/JAHA.121.023024 doi (DE-627)DOAJ081326386 (DE-599)DOAJ7a1b7a53140b46c492daf7cb0d63e6fc DE-627 ger DE-627 rakwb eng RC666-701 Natalia Campos‐Obando verfasserin aut Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system Ariadne Bosman verfasserin aut Maryam Kavousi verfasserin aut Carolina Medina‐Gomez verfasserin aut Bram C. J. van der Eerden verfasserin aut Daniel Bos verfasserin aut Oscar H. Franco verfasserin aut André G. Uitterlinden verfasserin aut M. Carola Zillikens verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 11(2022), 15 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:11 year:2022 number:15 https://doi.org/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 15
spelling	10.1161/JAHA.121.023024 doi (DE-627)DOAJ081326386 (DE-599)DOAJ7a1b7a53140b46c492daf7cb0d63e6fc DE-627 ger DE-627 rakwb eng RC666-701 Natalia Campos‐Obando verfasserin aut Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system Ariadne Bosman verfasserin aut Maryam Kavousi verfasserin aut Carolina Medina‐Gomez verfasserin aut Bram C. J. van der Eerden verfasserin aut Daniel Bos verfasserin aut Oscar H. Franco verfasserin aut André G. Uitterlinden verfasserin aut M. Carola Zillikens verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 11(2022), 15 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:11 year:2022 number:15 https://doi.org/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 15
allfields_unstemmed	10.1161/JAHA.121.023024 doi (DE-627)DOAJ081326386 (DE-599)DOAJ7a1b7a53140b46c492daf7cb0d63e6fc DE-627 ger DE-627 rakwb eng RC666-701 Natalia Campos‐Obando verfasserin aut Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system Ariadne Bosman verfasserin aut Maryam Kavousi verfasserin aut Carolina Medina‐Gomez verfasserin aut Bram C. J. van der Eerden verfasserin aut Daniel Bos verfasserin aut Oscar H. Franco verfasserin aut André G. Uitterlinden verfasserin aut M. Carola Zillikens verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 11(2022), 15 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:11 year:2022 number:15 https://doi.org/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 15
allfieldsGer	10.1161/JAHA.121.023024 doi (DE-627)DOAJ081326386 (DE-599)DOAJ7a1b7a53140b46c492daf7cb0d63e6fc DE-627 ger DE-627 rakwb eng RC666-701 Natalia Campos‐Obando verfasserin aut Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system Ariadne Bosman verfasserin aut Maryam Kavousi verfasserin aut Carolina Medina‐Gomez verfasserin aut Bram C. J. van der Eerden verfasserin aut Daniel Bos verfasserin aut Oscar H. Franco verfasserin aut André G. Uitterlinden verfasserin aut M. Carola Zillikens verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 11(2022), 15 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:11 year:2022 number:15 https://doi.org/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 15
allfieldsSound	10.1161/JAHA.121.023024 doi (DE-627)DOAJ081326386 (DE-599)DOAJ7a1b7a53140b46c492daf7cb0d63e6fc DE-627 ger DE-627 rakwb eng RC666-701 Natalia Campos‐Obando verfasserin aut Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed. chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system Ariadne Bosman verfasserin aut Maryam Kavousi verfasserin aut Carolina Medina‐Gomez verfasserin aut Bram C. J. van der Eerden verfasserin aut Daniel Bos verfasserin aut Oscar H. Franco verfasserin aut André G. Uitterlinden verfasserin aut M. Carola Zillikens verfasserin aut In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease Wiley, 2012 11(2022), 15 (DE-627)688605427 (DE-600)2653953-6 20479980 nnns volume:11 year:2022 number:15 https://doi.org/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc kostenfrei https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 kostenfrei https://doaj.org/toc/2047-9980 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 15
language	English
source	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 11(2022), 15 volume:11 year:2022 number:15
sourceStr	In Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease 11(2022), 15 volume:11 year:2022 number:15
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
authorswithroles_txt_mv	Natalia Campos‐Obando @@aut@@ Ariadne Bosman @@aut@@ Maryam Kavousi @@aut@@ Carolina Medina‐Gomez @@aut@@ Bram C. J. van der Eerden @@aut@@ Daniel Bos @@aut@@ Oscar H. Franco @@aut@@ André G. Uitterlinden @@aut@@ M. Carola Zillikens @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	688605427
id	DOAJ081326386
language_de	englisch
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Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. 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author	Natalia Campos‐Obando
spellingShingle	Natalia Campos‐Obando misc RC666-701 misc chronic kidney disease misc coronary artery calcification misc hyperphosphatemia misc Mendelian randomization misc phosphate misc Diseases of the circulatory (Cardiovascular) system Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study
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topic_title	RC666-701 Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study chronic kidney disease coronary artery calcification hyperphosphatemia Mendelian randomization phosphate
topic	misc RC666-701 misc chronic kidney disease misc coronary artery calcification misc hyperphosphatemia misc Mendelian randomization misc phosphate misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc chronic kidney disease misc coronary artery calcification misc hyperphosphatemia misc Mendelian randomization misc phosphate misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc chronic kidney disease misc coronary artery calcification misc hyperphosphatemia misc Mendelian randomization misc phosphate misc Diseases of the circulatory (Cardiovascular) system
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title	Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study
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title_full	Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study
author_sort	Natalia Campos‐Obando
journal	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
journalStr	Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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author_browse	Natalia Campos‐Obando Ariadne Bosman Maryam Kavousi Carolina Medina‐Gomez Bram C. J. van der Eerden Daniel Bos Oscar H. Franco André G. Uitterlinden M. Carola Zillikens
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author-letter	Natalia Campos‐Obando
doi_str_mv	10.1161/JAHA.121.023024
author2-role	verfasserin
title_sort	genetic evidence for a causal role of serum phosphate in coronary artery calcification: the rotterdam study
callnumber	RC666-701
title_auth	Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study
abstract	Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed.
abstractGer	Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed.
abstract_unstemmed	Background Hyperphosphatemia has been associated with coronary artery calcification (CAC) mostly in chronic kidney disease, but the association between phosphate levels within the normal phosphate range and CAC is unclear. Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. Further research into underlying mechanisms of this association and sex differences is needed.
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title_short	Genetic Evidence for a Causal Role of Serum Phosphate in Coronary Artery Calcification: The Rotterdam Study
url	https://doi.org/10.1161/JAHA.121.023024 https://doaj.org/article/7a1b7a53140b46c492daf7cb0d63e6fc https://www.ahajournals.org/doi/10.1161/JAHA.121.023024 https://doaj.org/toc/2047-9980
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author2	Ariadne Bosman Maryam Kavousi Carolina Medina‐Gomez Bram C. J. van der Eerden Daniel Bos Oscar H. Franco André G. Uitterlinden M. Carola Zillikens
author2Str	Ariadne Bosman Maryam Kavousi Carolina Medina‐Gomez Bram C. J. van der Eerden Daniel Bos Oscar H. Franco André G. Uitterlinden M. Carola Zillikens
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doi_str	10.1161/JAHA.121.023024
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up_date	2024-07-03T19:27:42.583Z
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Our objectives were to evaluate associations between phosphate levels and CAC among men and women from the general population and assess causality through Mendelian randomization. Methods and Results CAC, measured by electron‐beam computed tomography, and serum phosphate levels were assessed in 1889 individuals from the RS (Rotterdam Study). Phenotypic associations were tested through linear models adjusted for age, body mass index, blood pressure, smoking, prevalent cardiovascular disease and diabetes, 25‐hydroxyvitamin D, total calcium, C‐reactive protein, glucose, and total cholesterol : high‐density lipoprotein cholesterol ratio. Mendelian randomization was implemented through an allele score including 8 phosphate‐related single‐nucleotide polymorphisms. In phenotypic analyses, serum phosphate (per 1 SD) was associated with CAC with evidence for sex interaction (Pinteraction=0.003) (men β, 0.44 [95% CI, 0.30–0.59]; P=3×10−9; n=878; women β, 0.24 [95% CI, 0.08–0.40]; P=0.003; n=1011). Exclusion of hyperphosphatemia, chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m2) and prevalent cardiovascular disease yielded similar results. In Mendelian randomization analyses, instrumented phosphate was associated with CAC (total population β, 0.93 [95% CI: 0.07–1.79]; P=0.034; n=1693), even after exclusion of hyperphosphatemia, chronic kidney disease and prevalent cardiovascular disease (total population β, 1.23 [95% CI, 0.17–2.28]; P=0.023; n=1224). Conclusions Serum phosphate was associated with CAC in the general population with stronger effects in men. Mendelian randomization findings support a causal relation, also for serum phosphate and CAC in subjects without hyperphosphatemia, chronic kidney disease, and cardiovascular disease. 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