@article {8519,
	title = {{Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities: An Individual Participant Data Meta-analysis in a Global Consortium},
	journal = {Am J Kidney Dis},
	volume = {73},
	year = {2019},
	month = {02},
	pages = {206{\textendash}217},
	abstract = {Chronic kidney disease (CKD) is complicated by abnormalities that reflect disruption in filtration, tubular, and endocrine functions of the kidney. Our aim was to explore the relationship of specific laboratory result abnormalities and hypertension with the estimated glomerular filtration rate (eGFR) and albuminuria CKD staging framework.\ Cross-sectional individual participant-level analyses in a global consortium.\ 17 CKD and 38 general population and high-risk cohorts.\ Cohorts in the CKD Prognosis Consortium with data for eGFR and albuminuria, as well as a measurement of hemoglobin, bicarbonate, phosphorus, parathyroid hormone, potassium, or calcium, or hypertension.\ Data were obtained and analyzed between July 2015 and January 2018.\ We modeled the association of eGFR and albuminuria with hemoglobin, bicarbonate, phosphorus, parathyroid hormone, potassium, and calcium values using linear regression and with hypertension and categorical definitions of each abnormality using logistic regression. Results were pooled using random-effects meta-analyses.\ The CKD cohorts (n=254,666 participants) were 27\% women and 10\% black, with a mean age of 69 (SD, 12) years. The general population/high-risk cohorts (n=1,758,334) were 50\% women and 2\% black, with a mean age of 50 (16) years. There was a strong graded association between lower eGFR and all laboratory result abnormalities (ORs ranging from 3.27 [95\% CI, 2.68-3.97] to 8.91 [95\% CI, 7.22-10.99] comparing eGFRs of 15 to 29 with eGFRs of 45 to 59mL/min/1.73m2), whereas albuminuria had equivocal or weak associations with abnormalities (ORs ranging from 0.77 [95\% CI, 0.60-0.99] to 1.92 [95\% CI, 1.65-2.24] comparing urinary albumin-creatinine ratio > 300 vs < 30mg/g).\ Variations in study era, health care delivery system, typical diet, and laboratory assays.\ Lower eGFR was strongly associated with higher odds of multiple laboratory result abnormalities. Knowledge of risk associations might help guide management in the heterogeneous group of patients with CKD.},
	author = {Inker, L. A. and Grams, M. E. and Levey, A. S. and Coresh, J. and Cirillo, M. and Collins, J. F. and Gansevoort, R. T. and Gutierrez, O. M. and Hamano, T. and Heine, G. H. and Ishikawa, S. and Jee, S. H. and Kronenberg, F. and Landray, M. J. and Miura, K. and Nadkarni, G. N. and Peralta, C. A. and Rothenbacher, D. and Schaeffner, E. and Sedaghat, S. and Shlipak, M. G. and Zhang, L. and van Zuilen, A. D. and Hallan, S. I. and Kovesdy, C. P. and Woodward, M. and Levin, A. and Astor, B. and Appel, L. and Greene, T. and Chen, T. and Chalmers, J. and Woodward, M. and Arima, H. and Perkovic, V. and Yatsuya, H. and Tamakoshi, K. and Li, Y. and Hirakawa, Y. and Coresh, J. and Matsushita, K. and Grams, M. and Sang, Y. and Polkinghorne, K. and Chadban, S. and Atkins, R. and Levin, A. and Djurdjev, O. and Zhang, L. and Liu, L. and Zhao, M. and Wang, F. and Wang, J. and Schaeffner, E. and Ebert, N. and Martus, P. and Levin, A. and Djurdjev, O. and Tang, M. and Heine, G. and Emrich, I. and Seiler, S. and Zawada, A. and Nally, J. and Navaneethan, S. and Schold, J. and Zhang, L. and Zhao, M. and Wang, F. and Wang, J. and Shlipak, M. and Sarnak, M. and Katz, R. and Hiramoto, J. and Iso, H. and Yamagishi, K. and Umesawa, M. and Muraki, I. and Fukagawa, M. and Maruyama, S. and Hamano, T. and Hasegawa, T. and Fujii, N. and Wheeler, D. and Emberson, J. and Townend, J. and Landray, M. and Brenner, H. and Sch?ttker, B. and Saum, K. U. and Rothenbacher, D. and Fox, C. and Hwang, S. J. and K?ttgen, A. and Kronenberg, F. and Schneider, M. P. and Eckardt, K. U. and Green, J. and Kirchner, H. L. and Chang, A. R. and Ho, K. and Ito, S. and Miyazaki, M. and Nakayama, M. and Yamada, G. and Cirillo, M. and Irie, F. and Sairenchi, T. and Ishikawa, S. and Yano, Y. and Kotani, K. and Nakamura, T. and Jee, S. H. and Kimm, H. and Mok, Y. and Chodick, G. and Shalev, V. and Wetzels, J. F. M. and Blankestijn, P. J. and van Zuilen, A. D. and van den Brand, J. and Sarnak, M. and Inker, L. and Peralta, C. and Hiramoto, J. and Katz, R. and Sarnak, M. and Kronenberg, F. and Kollerits, B. and Ritz, E. and Nitsch, D. and Roderick, P. and Fletcher, A. and Bottinger, E. and Nadkarni, G. N. and Ellis, S. B. and Nadukuru, R. and Sang, Y. and Ueshima, H. and Okayama, A. and Miura, K. and Tanaka, S. and Ueshima, H. and Okamura, T. and Miura, K. and Tanaka, S. and Miura, K. and Okayama, A. and Kadota, A. and Tanaka, S. and Kenealy, T. and Elley, C. R. and Collins, J. F. and Drury, P. L. and Ohkubo, T. and Asayama, K. and Metoki, H. and Kikuya, M. and Nakayama, M. and Nelson, R. G. and Knowler, W. C. and Gansevoort, R. T. and Bakker, S. J. and Hak, E. and Heerspink, H. J. L. and Brunskill, N. and Major, R. and Shepherd, D. and Medcalf, J. and Jassal, S. K. and Bergstrom, J. and Ix, J. H. and Barrett-Connor, E. and Kovesdy, C. and Kalantar-Zadeh, K. and Sumida, K. and Gutierrez, O. M. and Muntner, P. and Warnock, D. and McClellan, W. and Heerspink, H. J. L. and de Zeeuw, D. and Brenner, B. and Sedaghat, S. and Ikram, M. A. and Hoorn, E. J. and Dehghan, A. and Carrero, J. J. and Gasparini, A. and Wettermark, B. and Elinder, C. G. and Wong, T. Y. and Sabanayagam, C. and Cheng, C. Y. and Visseren, F. L. J. and Evans, M. and Segelmark, M. and Stendahl, M. and Sch?n, S. and Tangri, N. and Sud, M. and Naimark, D. and Wen, C. P. and Tsao, C. K. and Tsai, M. K. and Chen, C. H. and Konta, T. and Hirayama, A. and Ichikawa, K. and Lannfelt, L. and Larsson, A. and ?rnl?v, J. and Bilo, H. J. G. and Landman, G. W. D. and van Hateren, K. J. J. and Kleefstra, N. and Coresh Chair, J. and Gansevoort, R. T. and Grams, M. E. and Hallan, S. and Kovesdy, C. P. and Levey, A. S. and Matsushita, K. and Shalev, V. and Woodward, M. and Ballew, S. H. and Chen, J. and Coresh, J. and Grams, M. E. and Kwak, L. and Matsushita, K. and Sang, Y. and Surapaneni, A. and Woodward, M.}
}
@article {8772,
	title = {{The trans-ancestral genomic architecture of glycemic traits},
	journal = {Nat Genet},
	volume = {53},
	year = {2021},
	month = {06},
	pages = {840{\textendash}860},
	abstract = {10.1038/s41588-021-00852-9Glycemic traits are used to diagnose and monitor type 2 diabetes and cardiometabolic health. To date, most genetic studies of glycemic traits have focused on individuals of European ancestry. Here we aggregated genome-wide association studies comprising up to 281,416 individuals without diabetes (30\% non-European ancestry) for whom fasting glucose, 2-h glucose after an oral glucose challenge, glycated hemoglobin and fasting insulin data were available. Trans-ancestry and single-ancestry meta-analyses identified 242 loci (99 novel; P < 5 {\texttimes} 10-8), 80\% of which had no significant evidence of between-ancestry heterogeneity. Analyses restricted to individuals of European ancestry with equivalent sample size would have led to 24 fewer new loci. Compared with single-ancestry analyses, equivalent-sized trans-ancestry fine-mapping reduced the number of estimated variants in 99\% credible sets by a median of 37.5\%. Genomic-feature, gene-expression and gene-set analyses revealed distinct biological signatures for each trait, highlighting different underlying biological pathways. Our results increase our understanding of diabetes pathophysiology by using trans-ancestry studies for improved power and resolution.},
	author = {Chen, J. and Spracklen, C. N. and Marenne, G. and Varshney, A. and Corbin, L. J. and Luan, J. and Willems, S. M. and Wu, Y. and Zhang, X. and Horikoshi, M. and Boutin, T. S. and M{\"a}gi, R. and Waage, J. and Li-Gao, R. and Chan, K. H. K. and Yao, J. and Anasanti, M. D. and Chu, A. Y. and Claringbould, A. and Heikkinen, J. and Hong, J. and Hottenga, J. J. and Huo, S. and Kaakinen, M. A. and Louie, T. and M{\"a}rz, W. and Moreno-Macias, H. and Ndungu, A. and Nelson, S. C. and Nolte, I. M. and North, K. E. and Raulerson, C. K. and Ray, D. and Rohde, R. and Rybin, D. and Schurmann, C. and Sim, X. and Southam, L. and Stewart, I. D. and Wang, C. A. and Wang, Y. and Wu, P. and Zhang, W. and Ahluwalia, T. S. and Appel, E. V. R. and Bielak, L. F. and Brody, J. A. and Burtt, N. P. and Cabrera, C. P. and Cade, B. E. and Chai, J. F. and Chai, X. and Chang, L. C. and Chen, C. H. and Chen, B. H. and Chitrala, K. N. and Chiu, Y. F. and de Haan, H. G. and Delgado, G. E. and Demirkan, A. and Duan, Q. and Engmann, J. and Fatumo, S. A. and Gay{\'a}n, J. and Giulianini, F. and Gong, J. H. and Gustafsson, S. and Hai, Y. and Hartwig, F. P. and He, J. and Heianza, Y. and Huang, T. and Huerta-Chagoya, A. and Hwang, M. Y. and Jensen, R. A. and Kawaguchi, T. and Kentistou, K. A. and Kim, Y. J. and Kleber, M. E. and Kooner, I. K. and Lai, S. and Lange, L. A. and Langefeld, C. D. and Lauzon, M. and Li, M. and Ligthart, S. and Liu, J. and Loh, M. and Long, J. and Lyssenko, V. and Mangino, M. and Marzi, C. and Montasser, M. E. and Nag, A. and Nakatochi, M. and Noce, D. and Noordam, R. and Pistis, G. and Preuss, M. and Raffield, L. and Rasmussen-Torvik, L. J. and Rich, S. S. and Robertson, N. R. and Rueedi, R. and Ryan, K. and Sanna, S. and Saxena, R. and Schraut, K. E. and Sennblad, B. and Setoh, K. and Smith, A. V. and Spars{\o}, T. and Strawbridge, R. J. and Takeuchi, F. and Tan, J. and Trompet, S. and van den Akker, E. and van der Most, P. J. and Verweij, N. and Vogel, M. and Wang, H. and Wang, C. and Wang, N. and Warren, H. R. and Wen, W. and Wilsgaard, T. and Wong, A. and Wood, A. R. and Xie, T. and Zafarmand, M. H. and Zhao, J. H. and Zhao, W. and Amin, N. and Arzumanyan, Z. and Astrup, A. and Bakker, S. J. L. and Baldassarre, D. and Beekman, M. and Bergman, R. N. and Bertoni, A. and Bl{\"u}her, M. and Bonnycastle, L. L. and Bornstein, S. R. and Bowden, D. W. and Cai, Q. and Campbell, A. and Campbell, H. and Chang, Y. C. and de Geus, E. J. C. and Dehghan, A. and Du, S. and Eiriksdottir, G. and Farmaki, A. E. and Fr{\r a}nberg, M. and Fuchsberger, C. and Gao, Y. and Gjesing, A. P. and Goel, A. and Han, S. and Hartman, C. A. and Herder, C. and Hicks, A. A. and Hsieh, C. H. and Hsueh, W. A. and Ichihara, S. and Igase, M. and Ikram, M. A. and Johnson, W. C. and J{\o}rgensen, M. E. and Joshi, P. K. and Kalyani, R. R. and Kandeel, F. R. and Katsuya, T. and Khor, C. C. and Kiess, W. and Kolcic, I. and Kuulasmaa, T. and Kuusisto, J. and L{\"a}ll, K. and Lam, K. and Lawlor, D. A. and Lee, N. R. and Lemaitre, R. N. and Li, H. and Lin, S. Y. and Lindstr{\"o}m, J. and Linneberg, A. and Liu, J. and Lorenzo, C. and Matsubara, T. and Matsuda, F. and Mingrone, G. and Mooijaart, S. and Moon, S. and Nabika, T. and Nadkarni, G. N. and Nadler, J. L. and Nelis, M. and Neville, M. J. and Norris, J. M. and Ohyagi, Y. and Peters, A. and Peyser, P. A. and Polasek, O. and Qi, Q. and Raven, D. and Reilly, D. F. and Reiner, A. and Rivideneira, F. and Roll, K. and Rudan, I. and Sabanayagam, C. and Sandow, K. and Sattar, N. and Sch{\"u}rmann, A. and Shi, J. and Stringham, H. M. and Taylor, K. D. and Teslovich, T. M. and Thuesen, B. and Timmers, P. R. H. J. and Tremoli, E. and Tsai, M. Y. and Uitterlinden, A. and van Dam, R. M. and van Heemst, D. and van Hylckama Vlieg, A. and Van Vliet-Ostaptchouk, J. V. and Vangipurapu, J. and Vestergaard, H. and Wang, T. and Willems van Dijk, K. and Zemunik, T. and Abecasis, G. R. and Adair, L. S. and Aguilar-Salinas, C. A. and Alarc{\'o}n-Riquelme, M. E. and An, P. and Aviles-Santa, L. and Becker, D. M. and Beilin, L. J. and Bergmann, S. and Bisgaard, H. and Black, C. and Boehnke, M. and Boerwinkle, E. and B{\"o}hm, B. O. and B{\o}nnelykke, K. and Boomsma, D. I. and Bottinger, E. P. and Buchanan, T. A. and Canouil, M. and Caulfield, M. J. and Chambers, J. C. and Chasman, D. I. and Chen, Y. I. and Cheng, C. Y. and Collins, F. S. and Correa, A. and Cucca, F. and de Silva, H. J. and Dedoussis, G. and Elmst{\r a}hl, S. and Evans, M. K. and Ferrannini, E. and Ferrucci, L. and Florez, J. C. and Franks, P. W. and Frayling, T. M. and Froguel, P. and Gigante, B. and Goodarzi, M. O. and Gordon-Larsen, P. and Grallert, H. and Grarup, N. and Grimsgaard, S. and Groop, L. and Gudnason, V. and Guo, X. and Hamsten, A. and Hansen, T. and Hayward, C. and Heckbert, S. R. and Horta, B. L. and Huang, W. and Ingelsson, E. and James, P. S. and Jarvelin, M. R. and Jonas, J. B. and Jukema, J. W. and Kaleebu, P. and Kaplan, R. and Kardia, S. L. R. and Kato, N. and Keinanen-Kiukaanniemi, S. M. and Kim, B. J. and Kivimaki, M. and Koistinen, H. A. and Kooner, J. S. and K{\"o}rner, A. and Kovacs, P. and Kuh, D. and Kumari, M. and Kutalik, Z. and Laakso, M. and Lakka, T. A. and Launer, L. J. and Leander, K. and Li, H. and Lin, X. and Lind, L. and Lindgren, C. and Liu, S. and Loos, R. J. F. and Magnusson, P. K. E. and Mahajan, A. and Metspalu, A. and Mook-Kanamori, D. O. and Mori, T. A. and Munroe, P. B. and Nj{\o}lstad, I. and O{\textquoteright}Connell, J. R. and Oldehinkel, A. J. and Ong, K. K. and Padmanabhan, S. and Palmer, C. N. A. and Palmer, N. D. and Pedersen, O. and Pennell, C. E. and Porteous, D. J. and Pramstaller, P. P. and Province, M. A. and Psaty, B. M. and Qi, L. and Raffel, L. J. and Rauramaa, R. and Redline, S. and Ridker, P. M. and Rosendaal, F. R. and Saaristo, T. E. and Sandhu, M. and Saramies, J. and Schneiderman, N. and Schwarz, P. and Scott, L. J. and Selvin, E. and Sever, P. and Shu, X. O. and Slagboom, P. E. and Small, K. S. and Smith, B. H. and Snieder, H. and Sofer, T. and S{\o}rensen, T. I. A. and Spector, T. D. and Stanton, A. and Steves, C. J. and Stumvoll, M. and Sun, L. and Tabara, Y. and Tai, E. S. and Timpson, N. J. and Tonjes, A. and Tuomilehto, J. and Tusie, T. and Uusitupa, M. and van der Harst, P. and van Duijn, C. and Vitart, V. and Vollenweider, P. and Vrijkotte, T. G. M. and Wagenknecht, L. E. and Walker, M. and Wang, Y. X. and Wareham, N. J. and Watanabe, R. M. and Watkins, H. and Wei, W. B. and Wickremasinghe, A. R. and Willemsen, G. and Wilson, J. F. and Wong, T. Y. and Wu, J. Y. and Xiang, A. H. and Yanek, L. R. and Yengo, L. and Yokota, M. and Zeggini, E. and Zheng, W. and Zonderman, A. B. and Rotter, J. I. and Gloyn, A. L. and McCarthy, M. I. and Dupuis, J. and Meigs, J. B. and Scott, R. A. and Prokopenko, I. and Leong, A. and Liu, C. T. and Parker, S. C. J. and Mohlke, K. L. and Langenberg, C. and Wheeler, E. and Morris, A. P. and Barroso, I. and de Haan, H. G. and van den Akker, E. and van der Most, P. J. and de Geus, E. J. C. and van Dam, R. M. and van Heemst, D. and van Hylckama Vlieg, A. and van Willems van Dijk, K. and de Silva, H. J. and van der Harst, P. and van Duijn, C.}
}
@article {9460,
	title = {{Trans Fatty Acid Biomarkers and Incident Type 2 Diabetes: Pooled Analysis of 12 Prospective Cohort Studies in the Fatty Acids and Outcomes Research Consortium (FORCE)},
	journal = {Diabetes Care},
	volume = {45},
	year = {2022},
	month = {Apr},
	pages = {854{\textendash}863},
	abstract = {Trans fatty acids (TFAs) have harmful biologic effects that could increase the risk of type 2 diabetes (T2D), but evidence remains uncertain. We aimed to investigate the prospective associations of TFA biomarkers and T2D by conducting an individual participant-level pooled analysis.\ 18 years without prevalent diabetes. Each cohort conducted de novo harmonized analyses using a prespecified protocol, and findings were pooled using inverse-variance weighted meta-analysis. Heterogeneity was explored by prespecified between-study and within-study characteristics.\ 0.1).\ Circulating individual trans-18:2 TFA biomarkers were not associated with risk of T2D, while trans-16:1n-9, total trans-18:1, and total trans-18:2 were inversely associated. Findings may reflect the influence of mixed TFA sources (industrial vs. natural ruminant), a general decline in TFA exposure due to policy changes during this period, or the relatively limited range of TFA levels.},
	author = {Lai, H. T. M. and Imamura, F. and Korat, A. V. A. and Murphy, R. A. and Tintle, N. and Bassett, J. K. and Chen, J. and ger, J. and Chien, K. L. and Senn, M. and Wood, A. C. and Forouhi, N. G. and Schulze, M. B. and Harris, W. S. and Vasan, R. S. and Hu, F. and Giles, G. G. and Hodge, A. and Djousse, L. and Brouwer, I. A. and Qian, F. and Sun, Q. and Wu, J. H. Y. and Marklund, M. and Lemaitre, R. N. and Siscovick, D. S. and Fretts, A. M. and Shadyab, A. H. and Manson, J. E. and Howard, B. V. and Robinson, J. G. and Wallace, R. B. and Wareham, N. J. and Chen, Y. I. and Rotter, J. I. and Tsai, M. Y. and Micha, R. and Mozaffarian, D.}
}
@article {9863,
	title = {{Multi-ancestry genome-wide association study reveals novel genetic signals for lung function decline},
	journal = {medRxiv},
	year = {2024},
	month = {Nov},
	abstract = {Accelerated decline in lung function contributes to the development of chronic respiratory disease. Despite evidence for a genetic component, few genetic associations with lung function decline have been identified.\ To evaluate genome-wide associations and putative downstream functionality of genetic variants with lung function decline in diverse general population cohorts.\ /FVC) in participants across six cohorts in the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium and the UK Biobank. Genotypes were imputed to TOPMed (CHARGE cohorts) or Haplotype Reference Consortium (HRC) (UK Biobank) reference panels, and GWAS analyses used generalized estimating equation models with robust standard error. Models were stratified by cohort, ancestry, and sex, and adjusted for important lung function confounders and genotype principal components. Results were combined in cross-ancestry and ancestry-specific meta-analyses. Selected top variants were tested for replication in two independent COPD-enriched cohorts.\ ) with consistent associations across ancestries or decline phenotypes. Annotation class analysis revealed significant enrichment of several regulatory processes for corticosteroid biosynthesis and metabolism. Drug repurposing analysis identified 43 approved compounds targeting eight of the implicated 38 genes.\ Our multi-ancestry GWAS meta-analyses identified numerous genetic loci associated with lung function decline. These findings contribute knowledge to the genetic architecture of lung function decline, provide evidence for a role of endogenous corticosteroids in the etiology of lung function decline, and identify drug targets that merit further study for potential repurposing to slow lung function decline and treat lung disease.},
	author = {Patchen, B. K. and Zhang, J. and Gaddis, N. and Bartz, T. M. and Chen, J. and Debban, C. and Leonard, H. and Nguyen, N. Q. and Seo, J. and Tern, C. and Allen, R. and DeMeo, D. L. and Fornage, M. and Melbourne, C. and Minto, M. and Moll, M. and O{\textquoteright}Connor, G. and Pottinger, T. and Psaty, B. M. and Rich, S. S. and Rotter, J. I. and Silverman, E. K. and Stratford, J. and Graham Barr, R. and Cho, M. H. and Gharib, S. A. and Manichaikul, A. and North, K. and Oelsner, E. C. and Simonsick, E. M. and Tobin, M. D. and Yu, B. and Choi, S. H. and Dupuis, J. and Cassano, P. A. and Hancock, D. B.}
}
