Cannabis Use and CKD: Epidemiological Associations and Mendelian Randomization
The association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS). Retrospective cohort study and...
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| Published in: | Kidney medicine Vol. 5; no. 2; p. 100582 |
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| Abstract | The association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS).
Retrospective cohort study and genome-wide association study.
The retrospective study was conducted on the All of Us cohort (N=223,354). Genetic instruments for cannabis use disorder were identified from 3 GWAS: the Psychiatric Genomics Consortium Substance Use Disorders, iPSYCH, and deCODE (N=384,032). Association between genetic instruments and CKD was investigated in the CKDGen GWAS (N>1.2 million).
Cannabis consumption.
CKD outcomes included: cystatin-C and creatinine-based kidney function, proteinuria, and blood urea nitrogen.
We conducted association analyses to test for frequency of cannabis use and CKD. To evaluate causality, we performed a 2-sample Mendelian randomization.
In the retrospective study, compared to former users, less than monthly (OR, 1.01; 95% CI, 0.87-1.18; P=0.87) and monthly cannabis users (OR, 1.15; 95% CI, 0.86-1.52; P=0.33) did not have higher CKD odds. Conversely, weekly (OR, 1.28; 95% CI, 1.01-1.60; P=0.04) and daily use (OR, 1.25; 95% CI, 1.04-1.50; P=0.02) was significantly associated with CKD, adjusted for multiple confounders. In Mendelian randomization, genetic liability to cannabis use disorder was not associated with increased odds for CKD (OR, 1.00; 95% CI, 0.99-1.01; P=0.96). These results were robust across different Mendelian randomization techniques and multiple kidney traits.
Likely underreporting of cannabis use. In Mendelian randomization, genetic instruments were identified in the GWAS that included individuals primarily of European ancestry.
Despite the epidemiological association between cannabis use and CKD, there was no evidence of a causal effect, indicating confounding in observational studies.
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| AbstractList | The association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS).
Retrospective cohort study and genome-wide association study.
The retrospective study was conducted on the All of Us cohort (N=223,354). Genetic instruments for cannabis use disorder were identified from 3 GWAS: the Psychiatric Genomics Consortium Substance Use Disorders, iPSYCH, and deCODE (N=384,032). Association between genetic instruments and CKD was investigated in the CKDGen GWAS (N>1.2 million).
Cannabis consumption.
CKD outcomes included: cystatin-C and creatinine-based kidney function, proteinuria, and blood urea nitrogen.
We conducted association analyses to test for frequency of cannabis use and CKD. To evaluate causality, we performed a 2-sample Mendelian randomization.
In the retrospective study, compared to former users, less than monthly (OR, 1.01; 95% CI, 0.87-1.18; P=0.87) and monthly cannabis users (OR, 1.15; 95% CI, 0.86-1.52; P=0.33) did not have higher CKD odds. Conversely, weekly (OR, 1.28; 95% CI, 1.01-1.60; P=0.04) and daily use (OR, 1.25; 95% CI, 1.04-1.50; P=0.02) was significantly associated with CKD, adjusted for multiple confounders. In Mendelian randomization, genetic liability to cannabis use disorder was not associated with increased odds for CKD (OR, 1.00; 95% CI, 0.99-1.01; P=0.96). These results were robust across different Mendelian randomization techniques and multiple kidney traits.
Likely underreporting of cannabis use. In Mendelian randomization, genetic instruments were identified in the GWAS that included individuals primarily of European ancestry.
Despite the epidemiological association between cannabis use and CKD, there was no evidence of a causal effect, indicating confounding in observational studies.
[Display omitted] The association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS).Rationale & ObjectiveThe association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS).Retrospective cohort study and genome-wide association study.Study DesignRetrospective cohort study and genome-wide association study.The retrospective study was conducted on the All of Us cohort (N=223,354). Genetic instruments for cannabis use disorder were identified from 3 GWAS: the Psychiatric Genomics Consortium Substance Use Disorders, iPSYCH, and deCODE (N=384,032). Association between genetic instruments and CKD was investigated in the CKDGen GWAS (N > 1.2 million).Setting & ParticipantsThe retrospective study was conducted on the All of Us cohort (N=223,354). Genetic instruments for cannabis use disorder were identified from 3 GWAS: the Psychiatric Genomics Consortium Substance Use Disorders, iPSYCH, and deCODE (N=384,032). Association between genetic instruments and CKD was investigated in the CKDGen GWAS (N > 1.2 million).Cannabis consumption.ExposureCannabis consumption.CKD outcomes included: cystatin-C and creatinine-based kidney function, proteinuria, and blood urea nitrogen.OutcomesCKD outcomes included: cystatin-C and creatinine-based kidney function, proteinuria, and blood urea nitrogen.We conducted association analyses to test for frequency of cannabis use and CKD. To evaluate causality, we performed a 2-sample Mendelian randomization.Analytical ApproachWe conducted association analyses to test for frequency of cannabis use and CKD. To evaluate causality, we performed a 2-sample Mendelian randomization.In the retrospective study, compared to former users, less than monthly (OR, 1.01; 95% CI, 0.87-1.18; P = 0.87) and monthly cannabis users (OR, 1.15; 95% CI, 0.86-1.52; P = 0.33) did not have higher CKD odds. Conversely, weekly (OR, 1.28; 95% CI, 1.01-1.60; P = 0.04) and daily use (OR, 1.25; 95% CI, 1.04-1.50; P = 0.02) was significantly associated with CKD, adjusted for multiple confounders. In Mendelian randomization, genetic liability to cannabis use disorder was not associated with increased odds for CKD (OR, 1.00; 95% CI, 0.99-1.01; P = 0.96). These results were robust across different Mendelian randomization techniques and multiple kidney traits.ResultsIn the retrospective study, compared to former users, less than monthly (OR, 1.01; 95% CI, 0.87-1.18; P = 0.87) and monthly cannabis users (OR, 1.15; 95% CI, 0.86-1.52; P = 0.33) did not have higher CKD odds. Conversely, weekly (OR, 1.28; 95% CI, 1.01-1.60; P = 0.04) and daily use (OR, 1.25; 95% CI, 1.04-1.50; P = 0.02) was significantly associated with CKD, adjusted for multiple confounders. In Mendelian randomization, genetic liability to cannabis use disorder was not associated with increased odds for CKD (OR, 1.00; 95% CI, 0.99-1.01; P = 0.96). These results were robust across different Mendelian randomization techniques and multiple kidney traits.Likely underreporting of cannabis use. In Mendelian randomization, genetic instruments were identified in the GWAS that included individuals primarily of European ancestry.LimitationsLikely underreporting of cannabis use. In Mendelian randomization, genetic instruments were identified in the GWAS that included individuals primarily of European ancestry.Despite the epidemiological association between cannabis use and CKD, there was no evidence of a causal effect, indicating confounding in observational studies.ConclusionsDespite the epidemiological association between cannabis use and CKD, there was no evidence of a causal effect, indicating confounding in observational studies. The association between cannabis use and chronic kidney disease (CKD) is controversial. We aimed to assess association of CKD with cannabis use in a large cohort study and then assess causality using Mendelian randomization with a genome-wide association study (GWAS). Retrospective cohort study and genome-wide association study. The retrospective study was conducted on the All of Us cohort (N=223,354). Genetic instruments for cannabis use disorder were identified from 3 GWAS: the Psychiatric Genomics Consortium Substance Use Disorders, iPSYCH, and deCODE (N=384,032). Association between genetic instruments and CKD was investigated in the CKDGen GWAS (N > 1.2 million). Cannabis consumption. CKD outcomes included: cystatin-C and creatinine-based kidney function, proteinuria, and blood urea nitrogen. We conducted association analyses to test for frequency of cannabis use and CKD. To evaluate causality, we performed a 2-sample Mendelian randomization. In the retrospective study, compared to former users, less than monthly (OR, 1.01; 95% CI, 0.87-1.18; = 0.87) and monthly cannabis users (OR, 1.15; 95% CI, 0.86-1.52; = 0.33) did not have higher CKD odds. Conversely, weekly (OR, 1.28; 95% CI, 1.01-1.60; = 0.04) and daily use (OR, 1.25; 95% CI, 1.04-1.50; = 0.02) was significantly associated with CKD, adjusted for multiple confounders. In Mendelian randomization, genetic liability to cannabis use disorder was not associated with increased odds for CKD (OR, 1.00; 95% CI, 0.99-1.01; = 0.96). These results were robust across different Mendelian randomization techniques and multiple kidney traits. Likely underreporting of cannabis use. In Mendelian randomization, genetic instruments were identified in the GWAS that included individuals primarily of European ancestry. Despite the epidemiological association between cannabis use and CKD, there was no evidence of a causal effect, indicating confounding in observational studies. |
| ArticleNumber | 100582 |
| Author | Rajagopal, Madhumitha Kamat, Samir O’Hagan, Ross Rein, Joshua L. Coca, Steven Charney, Alexander W. Nadkarni, Girish N. Gulamali, Faris Paranjpe, Ishan Dellepiane, Sergio Do, Ron Glicksberg, Benjamin S. |
| Author_xml | – sequence: 1 givenname: Sergio orcidid: 0000-0002-7133-4740 surname: Dellepiane fullname: Dellepiane, Sergio organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 2 givenname: Ishan surname: Paranjpe fullname: Paranjpe, Ishan organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 3 givenname: Madhumitha surname: Rajagopal fullname: Rajagopal, Madhumitha organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 4 givenname: Samir surname: Kamat fullname: Kamat, Samir organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 5 givenname: Ross surname: O’Hagan fullname: O’Hagan, Ross organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 6 givenname: Faris surname: Gulamali fullname: Gulamali, Faris organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 7 givenname: Joshua L. surname: Rein fullname: Rein, Joshua L. organization: Department of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 8 givenname: Alexander W. surname: Charney fullname: Charney, Alexander W. organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 9 givenname: Ron surname: Do fullname: Do, Ron organization: Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 10 givenname: Steven surname: Coca fullname: Coca, Steven organization: Hasso Plattner Institute for Digital Health at Mount Sinai, Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 11 givenname: Benjamin S. surname: Glicksberg fullname: Glicksberg, Benjamin S. organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY – sequence: 12 givenname: Girish N. surname: Nadkarni fullname: Nadkarni, Girish N. email: girish.nadkarni@mountsinai.org organization: Mount Sinai Clinical Intelligence Center (MSCIC), Icahn School of Medicine at Mount Sinai, New York, NY |
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| Keywords | Cannabis chronic kidney disease Mendelian randomization |
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| Title | Cannabis Use and CKD: Epidemiological Associations and Mendelian Randomization |
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