Medical Records-Based Genetic Studies of the Complement System
Genetic variants in complement genes have been associated with a wide range of human disease states, but well-powered genetic association studies of complement activation have not been performed in large multiethnic cohorts. We performed medical records-based genome-wide and phenome-wide association...
Gespeichert in:
| Veröffentlicht in: | Journal of the American Society of Nephrology 2021-08, Vol.32 (8), p.2031-2047 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2047 |
|---|---|
| container_issue | 8 |
| container_start_page | 2031 |
| container_title | Journal of the American Society of Nephrology |
| container_volume | 32 |
| creator | Khan, Atlas Shang, Ning Petukhova, Lynn Zhang, Jun Shen, Yufeng Hebbring, Scott J Moncrieffe, Halima Kottyan, Leah C Namjou-Khales, Bahram Knevel, Rachel Raychaudhuri, Soumya Karlson, Elizabeth W Harley, John B Stanaway, Ian B Crosslin, David Denny, Joshua C Elkind, Mitchell S V Gharavi, Ali G Hripcsak, George Weng, Chunhua Kiryluk, Krzysztof |
| description | Genetic variants in complement genes have been associated with a wide range of human disease states, but well-powered genetic association studies of complement activation have not been performed in large multiethnic cohorts.
We performed medical records-based genome-wide and phenome-wide association studies for plasma C3 and C4 levels among participants of the Electronic Medical Records and Genomics (eMERGE) network.
In a GWAS for C3 levels in 3949 individuals, we detected two genome-wide significant loci: chr.1q31.3 (CFH locus; rs3753396-A;
=0.20; 95% CI, 0.14 to 0.25;
=1.52x10
) and chr.19p13.3 (C3 locus; rs11569470-G;
=0.19; 95% CI, 0.13 to 0.24;
=1.29x10
). These two loci explained approximately 2% of variance in C3 levels. GWAS for C4 levels involved 3998 individuals and revealed a genome-wide significant locus at chr.6p21.32 (C4 locus; rs3135353-C;
=0.40; 95% CI, 0.34 to 0.45;
=4.58x10
). This locus explained approximately 13% of variance in C4 levels. The multiallelic copy number variant analysis defined two structural genomic C4 variants with large effect on blood C4 levels: C4-BS (
=-0.36; 95% CI, -0.42 to -0.30;
=2.98x10
) and C4-AL-BS (
=0.25; 95% CI, 0.21 to 0.29;
=8.11x10
). Overall, C4 levels were strongly correlated with copy numbers of C4A and C4B genes. In comprehensive phenome-wide association studies involving 102,138 eMERGE participants, we cataloged a full spectrum of autoimmune, cardiometabolic, and kidney diseases genetically related to systemic complement activation.
We discovered genetic determinants of plasma C3 and C4 levels using eMERGE genomic data linked to electronic medical records. Genetic variants regulating C3 and C4 levels have large effects and multiple clinical correlations across the spectrum of complement-related diseases in humans. |
| doi_str_mv | 10.1681/asn.2020091371 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8455263</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2522189835</sourcerecordid><originalsourceid>FETCH-LOGICAL-c501t-215d601e7951cb9c71a58741a42392c6664bb26d0a92d378f6d2a16c2fa7c9203</originalsourceid><addsrcrecordid>eNpVkEtPwzAQhC0EoqVw5Yhy5JLitWM7uVQqFRSkAhKFs-XYGxqUR4kTpP57gloKnHalnZkdfYScAx2DjOHK-GrMKKM0Aa7ggAxBcB7ySNDDfqeRDKVUfEBOvH-nFART6pgMOE8ikDQekskDutyaInhGWzfOh9fGowvmWGGb22DZdi5HH9RZ0K4wmNXlusASqzZYbnyL5Sk5ykzh8Ww3R-T19uZldhcunub3s-kitIJCGzIQTlJAlQiwaWIVGBGrCEzEeMKslDJKUyYdNQlzXMWZdMyAtCwzyiaM8hGZbHPXXVqis32DxhR63eSlaTa6Nrn-f6nylX6rP3UcCcEk7wMudwFN_dGhb3WZe4tFYSqsO6-ZYAziJOail463UtvU3jeY7d8A1d_Q9XT5qH-h94aLv-X28h_K_Av74XxQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2522189835</pqid></control><display><type>article</type><title>Medical Records-Based Genetic Studies of the Complement System</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Khan, Atlas ; Shang, Ning ; Petukhova, Lynn ; Zhang, Jun ; Shen, Yufeng ; Hebbring, Scott J ; Moncrieffe, Halima ; Kottyan, Leah C ; Namjou-Khales, Bahram ; Knevel, Rachel ; Raychaudhuri, Soumya ; Karlson, Elizabeth W ; Harley, John B ; Stanaway, Ian B ; Crosslin, David ; Denny, Joshua C ; Elkind, Mitchell S V ; Gharavi, Ali G ; Hripcsak, George ; Weng, Chunhua ; Kiryluk, Krzysztof</creator><creatorcontrib>Khan, Atlas ; Shang, Ning ; Petukhova, Lynn ; Zhang, Jun ; Shen, Yufeng ; Hebbring, Scott J ; Moncrieffe, Halima ; Kottyan, Leah C ; Namjou-Khales, Bahram ; Knevel, Rachel ; Raychaudhuri, Soumya ; Karlson, Elizabeth W ; Harley, John B ; Stanaway, Ian B ; Crosslin, David ; Denny, Joshua C ; Elkind, Mitchell S V ; Gharavi, Ali G ; Hripcsak, George ; Weng, Chunhua ; Kiryluk, Krzysztof</creatorcontrib><description>Genetic variants in complement genes have been associated with a wide range of human disease states, but well-powered genetic association studies of complement activation have not been performed in large multiethnic cohorts.
We performed medical records-based genome-wide and phenome-wide association studies for plasma C3 and C4 levels among participants of the Electronic Medical Records and Genomics (eMERGE) network.
In a GWAS for C3 levels in 3949 individuals, we detected two genome-wide significant loci: chr.1q31.3 (CFH locus; rs3753396-A;
=0.20; 95% CI, 0.14 to 0.25;
=1.52x10
) and chr.19p13.3 (C3 locus; rs11569470-G;
=0.19; 95% CI, 0.13 to 0.24;
=1.29x10
). These two loci explained approximately 2% of variance in C3 levels. GWAS for C4 levels involved 3998 individuals and revealed a genome-wide significant locus at chr.6p21.32 (C4 locus; rs3135353-C;
=0.40; 95% CI, 0.34 to 0.45;
=4.58x10
). This locus explained approximately 13% of variance in C4 levels. The multiallelic copy number variant analysis defined two structural genomic C4 variants with large effect on blood C4 levels: C4-BS (
=-0.36; 95% CI, -0.42 to -0.30;
=2.98x10
) and C4-AL-BS (
=0.25; 95% CI, 0.21 to 0.29;
=8.11x10
). Overall, C4 levels were strongly correlated with copy numbers of C4A and C4B genes. In comprehensive phenome-wide association studies involving 102,138 eMERGE participants, we cataloged a full spectrum of autoimmune, cardiometabolic, and kidney diseases genetically related to systemic complement activation.
We discovered genetic determinants of plasma C3 and C4 levels using eMERGE genomic data linked to electronic medical records. Genetic variants regulating C3 and C4 levels have large effects and multiple clinical correlations across the spectrum of complement-related diseases in humans.</description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/asn.2020091371</identifier><identifier>PMID: 33941608</identifier><language>eng</language><publisher>United States: American Society of Nephrology</publisher><subject>Adult ; Aged ; Alleles ; Clinical Research ; Complement Activation - genetics ; Complement C3 - genetics ; Complement C3 - metabolism ; Complement C4 - genetics ; Complement C4 - metabolism ; Databases, Genetic ; Epidemiologic Studies ; Female ; Gene Dosage ; Genetic Loci ; Genetic Variation ; Genome-Wide Association Study ; Humans ; Male ; Medical Record Linkage ; Medical Records ; Middle Aged ; Young Adult</subject><ispartof>Journal of the American Society of Nephrology, 2021-08, Vol.32 (8), p.2031-2047</ispartof><rights>Copyright © 2021 by the American Society of Nephrology.</rights><rights>Copyright © 2021 by the American Society of Nephrology 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-215d601e7951cb9c71a58741a42392c6664bb26d0a92d378f6d2a16c2fa7c9203</citedby><cites>FETCH-LOGICAL-c501t-215d601e7951cb9c71a58741a42392c6664bb26d0a92d378f6d2a16c2fa7c9203</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8455263/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8455263/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33941608$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Khan, Atlas</creatorcontrib><creatorcontrib>Shang, Ning</creatorcontrib><creatorcontrib>Petukhova, Lynn</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Shen, Yufeng</creatorcontrib><creatorcontrib>Hebbring, Scott J</creatorcontrib><creatorcontrib>Moncrieffe, Halima</creatorcontrib><creatorcontrib>Kottyan, Leah C</creatorcontrib><creatorcontrib>Namjou-Khales, Bahram</creatorcontrib><creatorcontrib>Knevel, Rachel</creatorcontrib><creatorcontrib>Raychaudhuri, Soumya</creatorcontrib><creatorcontrib>Karlson, Elizabeth W</creatorcontrib><creatorcontrib>Harley, John B</creatorcontrib><creatorcontrib>Stanaway, Ian B</creatorcontrib><creatorcontrib>Crosslin, David</creatorcontrib><creatorcontrib>Denny, Joshua C</creatorcontrib><creatorcontrib>Elkind, Mitchell S V</creatorcontrib><creatorcontrib>Gharavi, Ali G</creatorcontrib><creatorcontrib>Hripcsak, George</creatorcontrib><creatorcontrib>Weng, Chunhua</creatorcontrib><creatorcontrib>Kiryluk, Krzysztof</creatorcontrib><title>Medical Records-Based Genetic Studies of the Complement System</title><title>Journal of the American Society of Nephrology</title><addtitle>J Am Soc Nephrol</addtitle><description>Genetic variants in complement genes have been associated with a wide range of human disease states, but well-powered genetic association studies of complement activation have not been performed in large multiethnic cohorts.
We performed medical records-based genome-wide and phenome-wide association studies for plasma C3 and C4 levels among participants of the Electronic Medical Records and Genomics (eMERGE) network.
In a GWAS for C3 levels in 3949 individuals, we detected two genome-wide significant loci: chr.1q31.3 (CFH locus; rs3753396-A;
=0.20; 95% CI, 0.14 to 0.25;
=1.52x10
) and chr.19p13.3 (C3 locus; rs11569470-G;
=0.19; 95% CI, 0.13 to 0.24;
=1.29x10
). These two loci explained approximately 2% of variance in C3 levels. GWAS for C4 levels involved 3998 individuals and revealed a genome-wide significant locus at chr.6p21.32 (C4 locus; rs3135353-C;
=0.40; 95% CI, 0.34 to 0.45;
=4.58x10
). This locus explained approximately 13% of variance in C4 levels. The multiallelic copy number variant analysis defined two structural genomic C4 variants with large effect on blood C4 levels: C4-BS (
=-0.36; 95% CI, -0.42 to -0.30;
=2.98x10
) and C4-AL-BS (
=0.25; 95% CI, 0.21 to 0.29;
=8.11x10
). Overall, C4 levels were strongly correlated with copy numbers of C4A and C4B genes. In comprehensive phenome-wide association studies involving 102,138 eMERGE participants, we cataloged a full spectrum of autoimmune, cardiometabolic, and kidney diseases genetically related to systemic complement activation.
We discovered genetic determinants of plasma C3 and C4 levels using eMERGE genomic data linked to electronic medical records. Genetic variants regulating C3 and C4 levels have large effects and multiple clinical correlations across the spectrum of complement-related diseases in humans.</description><subject>Adult</subject><subject>Aged</subject><subject>Alleles</subject><subject>Clinical Research</subject><subject>Complement Activation - genetics</subject><subject>Complement C3 - genetics</subject><subject>Complement C3 - metabolism</subject><subject>Complement C4 - genetics</subject><subject>Complement C4 - metabolism</subject><subject>Databases, Genetic</subject><subject>Epidemiologic Studies</subject><subject>Female</subject><subject>Gene Dosage</subject><subject>Genetic Loci</subject><subject>Genetic Variation</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Male</subject><subject>Medical Record Linkage</subject><subject>Medical Records</subject><subject>Middle Aged</subject><subject>Young Adult</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkEtPwzAQhC0EoqVw5Yhy5JLitWM7uVQqFRSkAhKFs-XYGxqUR4kTpP57gloKnHalnZkdfYScAx2DjOHK-GrMKKM0Aa7ggAxBcB7ySNDDfqeRDKVUfEBOvH-nFART6pgMOE8ikDQekskDutyaInhGWzfOh9fGowvmWGGb22DZdi5HH9RZ0K4wmNXlusASqzZYbnyL5Sk5ykzh8Ww3R-T19uZldhcunub3s-kitIJCGzIQTlJAlQiwaWIVGBGrCEzEeMKslDJKUyYdNQlzXMWZdMyAtCwzyiaM8hGZbHPXXVqis32DxhR63eSlaTa6Nrn-f6nylX6rP3UcCcEk7wMudwFN_dGhb3WZe4tFYSqsO6-ZYAziJOail463UtvU3jeY7d8A1d_Q9XT5qH-h94aLv-X28h_K_Av74XxQ</recordid><startdate>202108</startdate><enddate>202108</enddate><creator>Khan, Atlas</creator><creator>Shang, Ning</creator><creator>Petukhova, Lynn</creator><creator>Zhang, Jun</creator><creator>Shen, Yufeng</creator><creator>Hebbring, Scott J</creator><creator>Moncrieffe, Halima</creator><creator>Kottyan, Leah C</creator><creator>Namjou-Khales, Bahram</creator><creator>Knevel, Rachel</creator><creator>Raychaudhuri, Soumya</creator><creator>Karlson, Elizabeth W</creator><creator>Harley, John B</creator><creator>Stanaway, Ian B</creator><creator>Crosslin, David</creator><creator>Denny, Joshua C</creator><creator>Elkind, Mitchell S V</creator><creator>Gharavi, Ali G</creator><creator>Hripcsak, George</creator><creator>Weng, Chunhua</creator><creator>Kiryluk, Krzysztof</creator><general>American Society of Nephrology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202108</creationdate><title>Medical Records-Based Genetic Studies of the Complement System</title><author>Khan, Atlas ; Shang, Ning ; Petukhova, Lynn ; Zhang, Jun ; Shen, Yufeng ; Hebbring, Scott J ; Moncrieffe, Halima ; Kottyan, Leah C ; Namjou-Khales, Bahram ; Knevel, Rachel ; Raychaudhuri, Soumya ; Karlson, Elizabeth W ; Harley, John B ; Stanaway, Ian B ; Crosslin, David ; Denny, Joshua C ; Elkind, Mitchell S V ; Gharavi, Ali G ; Hripcsak, George ; Weng, Chunhua ; Kiryluk, Krzysztof</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-215d601e7951cb9c71a58741a42392c6664bb26d0a92d378f6d2a16c2fa7c9203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Alleles</topic><topic>Clinical Research</topic><topic>Complement Activation - genetics</topic><topic>Complement C3 - genetics</topic><topic>Complement C3 - metabolism</topic><topic>Complement C4 - genetics</topic><topic>Complement C4 - metabolism</topic><topic>Databases, Genetic</topic><topic>Epidemiologic Studies</topic><topic>Female</topic><topic>Gene Dosage</topic><topic>Genetic Loci</topic><topic>Genetic Variation</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Male</topic><topic>Medical Record Linkage</topic><topic>Medical Records</topic><topic>Middle Aged</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khan, Atlas</creatorcontrib><creatorcontrib>Shang, Ning</creatorcontrib><creatorcontrib>Petukhova, Lynn</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><creatorcontrib>Shen, Yufeng</creatorcontrib><creatorcontrib>Hebbring, Scott J</creatorcontrib><creatorcontrib>Moncrieffe, Halima</creatorcontrib><creatorcontrib>Kottyan, Leah C</creatorcontrib><creatorcontrib>Namjou-Khales, Bahram</creatorcontrib><creatorcontrib>Knevel, Rachel</creatorcontrib><creatorcontrib>Raychaudhuri, Soumya</creatorcontrib><creatorcontrib>Karlson, Elizabeth W</creatorcontrib><creatorcontrib>Harley, John B</creatorcontrib><creatorcontrib>Stanaway, Ian B</creatorcontrib><creatorcontrib>Crosslin, David</creatorcontrib><creatorcontrib>Denny, Joshua C</creatorcontrib><creatorcontrib>Elkind, Mitchell S V</creatorcontrib><creatorcontrib>Gharavi, Ali G</creatorcontrib><creatorcontrib>Hripcsak, George</creatorcontrib><creatorcontrib>Weng, Chunhua</creatorcontrib><creatorcontrib>Kiryluk, Krzysztof</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American Society of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khan, Atlas</au><au>Shang, Ning</au><au>Petukhova, Lynn</au><au>Zhang, Jun</au><au>Shen, Yufeng</au><au>Hebbring, Scott J</au><au>Moncrieffe, Halima</au><au>Kottyan, Leah C</au><au>Namjou-Khales, Bahram</au><au>Knevel, Rachel</au><au>Raychaudhuri, Soumya</au><au>Karlson, Elizabeth W</au><au>Harley, John B</au><au>Stanaway, Ian B</au><au>Crosslin, David</au><au>Denny, Joshua C</au><au>Elkind, Mitchell S V</au><au>Gharavi, Ali G</au><au>Hripcsak, George</au><au>Weng, Chunhua</au><au>Kiryluk, Krzysztof</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Medical Records-Based Genetic Studies of the Complement System</atitle><jtitle>Journal of the American Society of Nephrology</jtitle><addtitle>J Am Soc Nephrol</addtitle><date>2021-08</date><risdate>2021</risdate><volume>32</volume><issue>8</issue><spage>2031</spage><epage>2047</epage><pages>2031-2047</pages><issn>1046-6673</issn><eissn>1533-3450</eissn><abstract>Genetic variants in complement genes have been associated with a wide range of human disease states, but well-powered genetic association studies of complement activation have not been performed in large multiethnic cohorts.
We performed medical records-based genome-wide and phenome-wide association studies for plasma C3 and C4 levels among participants of the Electronic Medical Records and Genomics (eMERGE) network.
In a GWAS for C3 levels in 3949 individuals, we detected two genome-wide significant loci: chr.1q31.3 (CFH locus; rs3753396-A;
=0.20; 95% CI, 0.14 to 0.25;
=1.52x10
) and chr.19p13.3 (C3 locus; rs11569470-G;
=0.19; 95% CI, 0.13 to 0.24;
=1.29x10
). These two loci explained approximately 2% of variance in C3 levels. GWAS for C4 levels involved 3998 individuals and revealed a genome-wide significant locus at chr.6p21.32 (C4 locus; rs3135353-C;
=0.40; 95% CI, 0.34 to 0.45;
=4.58x10
). This locus explained approximately 13% of variance in C4 levels. The multiallelic copy number variant analysis defined two structural genomic C4 variants with large effect on blood C4 levels: C4-BS (
=-0.36; 95% CI, -0.42 to -0.30;
=2.98x10
) and C4-AL-BS (
=0.25; 95% CI, 0.21 to 0.29;
=8.11x10
). Overall, C4 levels were strongly correlated with copy numbers of C4A and C4B genes. In comprehensive phenome-wide association studies involving 102,138 eMERGE participants, we cataloged a full spectrum of autoimmune, cardiometabolic, and kidney diseases genetically related to systemic complement activation.
We discovered genetic determinants of plasma C3 and C4 levels using eMERGE genomic data linked to electronic medical records. Genetic variants regulating C3 and C4 levels have large effects and multiple clinical correlations across the spectrum of complement-related diseases in humans.</abstract><cop>United States</cop><pub>American Society of Nephrology</pub><pmid>33941608</pmid><doi>10.1681/asn.2020091371</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1046-6673 |
| ispartof | Journal of the American Society of Nephrology, 2021-08, Vol.32 (8), p.2031-2047 |
| issn | 1046-6673 1533-3450 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8455263 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Adult Aged Alleles Clinical Research Complement Activation - genetics Complement C3 - genetics Complement C3 - metabolism Complement C4 - genetics Complement C4 - metabolism Databases, Genetic Epidemiologic Studies Female Gene Dosage Genetic Loci Genetic Variation Genome-Wide Association Study Humans Male Medical Record Linkage Medical Records Middle Aged Young Adult |
| title | Medical Records-Based Genetic Studies of the Complement System |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T22%3A12%3A23IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Medical%20Records-Based%20Genetic%20Studies%20of%20the%20Complement%20System&rft.jtitle=Journal%20of%20the%20American%20Society%20of%20Nephrology&rft.au=Khan,%20Atlas&rft.date=2021-08&rft.volume=32&rft.issue=8&rft.spage=2031&rft.epage=2047&rft.pages=2031-2047&rft.issn=1046-6673&rft.eissn=1533-3450&rft_id=info:doi/10.1681/asn.2020091371&rft_dat=%3Cproquest_pubme%3E2522189835%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2522189835&rft_id=info:pmid/33941608&rfr_iscdi=true |