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@ARTICLE{Gaziano:182352,
      author       = {L. Gaziano and L. Sun and M. Arnold and S. Bell and K. Cho
                      and S. K. Kaptoge and R. J. Song and S. Burgess and D. C.
                      Posner and K. Mosconi and C. Robinson-Cohen and A. Mason and
                      T. R. Bolton and R. Tao and E. Allara and P. Schubert and L.
                      Chen and J. R. Staley and N. Staplin and S. Altay and P.
                      Amiano and V. Arndt$^*$ and J. Ärnlöv and E. L. M. Barr
                      and C. Björkelund and J. M. A. Boer and H. Brenner and E.
                      Casiglia and P. Chiodini and J. A. Cooper and J. Coresh and
                      M. Cushman and R. Dankner and K. W. Davidson and R. T. de
                      Jongh and C. Donfrancesco and G. Engström and H. Freisling
                      and A. G. de la Cámara and V. Gudnason and G. J. Hankey and
                      P.-O. Hansson and A. K. Heath and E. J. Hoorn and H. Imano
                      and S. K. Jassal$^*$ and R. Kaaks$^*$ and V. Katzke$^*$ and
                      J. Kauhanen and S. Kiechl and W. Koenig and R. A. Kronmal
                      and C. Kyrø and D. A. Lawlor and B. Ljungberg and C.
                      MacDonald and G. Masala and C. Meisinger and O. Melander and
                      C. Moreno Iribas and T. Ninomiya and D. Nitsch and B. G.
                      Nordestgaard and C. Onland-Moret and L. Palmieri and D.
                      Petrova and J. R. Q. Garcia and A. Rosengren and C.
                      Sacerdote and M. Sakurai and C. Santiuste and M. B. Schulze
                      and S. Sieri and J. Sundström and V. Tikhonoff and A.
                      Tjønneland and T. Tong and R. Tumino and I. Tzoulaki and Y.
                      T. van der Schouw and W. M. Monique Verschuren and H.
                      Völzke and R. B. Wallace and S. Goya Wannamethee and E.
                      Weiderpass and P. Willeit and M. Woodward and K. Yamagishi
                      and R. Zamora-Ros and E. A. Akwo and S. Pyarajan and D. R.
                      Gagnon and P. S. Tsao and S. Muralidhar and T. L. Edwards
                      and S. M. Damrauer and J. Joseph and L. Pennells and P. W.
                      F. Wilson and S. Harrison and T. A. Gaziano and M. Inouye
                      and C. Baigent and J. P. Casas and C. Langenberg and N.
                      Wareham and E. Riboli and J. Michael Gaziano and J. Danesh
                      and A. M. Hung and A. S. Butterworth and A. M. Wood and E.
                      Di Angelantonio and A. Koettgen and J. Shaw and R. Atkins
                      and P. Zimmet and P. Whincup and J. Willeit and C. Leitner
                      and P. Schnohr and S. Afzal and D. L. Pablos and C. M.
                      Arriscado and C. R. Ferreiro and H. Stocker and B.
                      Schöttker and B. Holleczek and A. Chetrit and L. Welin and
                      K. Svärdsudd and L. Welin and K. Svärdsudd and L. Lissner
                      and D. Hange and K. Mehlig and D. Nagel and P. E. Norman and
                      O. Almeida and L. Flicker and J. Hata and T. Honda and Y.
                      Furuta and H. Iso and A. Kitamura and I. Muraki and J. T.
                      Salonen and T.-P. Tuomainen and E. M. van Zutphen and N. M.
                      van Schoor and C. Lo Noce and G. Lappas and P. M. Nilsson
                      and B. Hedblad and J. Shaffer and J. Schwartz and D. Shimbo
                      and S. Sato and H. Iso and M. Hayama-Terada and T. Aspelund
                      and B. Thorsson and G. Sigurdsson and L. Chaker and K. M.
                      Ikram and M. Kavousi and H. Tunstall-Pedoe and G. Can and H.
                      Yüksel and U. Özkan and H. Nakagawa and Y. Morikawa and M.
                      Ishizaki and E. Feskens and J. M. Geleijnse and D. Kromhout},
      title        = {{M}ild-to-{M}oderate {K}idney {D}ysfunction and
                      {C}ardiovascular {D}isease: {O}bservational and {M}endelian
                      {R}andomization {A}nalyses},
      journal      = {Circulation},
      volume       = {146},
      number       = {20},
      issn         = {0009-7322},
      address      = {[S.l.]},
      publisher    = {Ovid},
      reportid     = {DKFZ-2022-02595},
      pages        = {1507-1517},
      year         = {2022},
      note         = {2022 Nov 15;146(20):1507-1517},
      abstract     = {Background: End-stage renal disease is associated with a
                      high risk of cardiovascular events. It is unknown, however,
                      whether mild-to-moderate kidney dysfunction is causally
                      related to coronary heart disease (CHD) and stroke.Methods:
                      Observational analyses were conducted using individual-level
                      data from 4 population data sources (Emerging Risk Factors
                      Collaboration, EPIC-CVD [European Prospective Investigation
                      into Cancer and Nutrition-Cardiovascular Disease Study],
                      Million Veteran Program, and UK Biobank), comprising 648 135
                      participants with no history of cardiovascular disease or
                      diabetes at baseline, yielding 42 858 and 15 693 incident
                      CHD and stroke events, respectively, during 6.8 million
                      person-years of follow-up. Using a genetic risk score of 218
                      variants for estimated glomerular filtration rate (eGFR), we
                      conducted Mendelian randomization analyses involving 413 718
                      participants (25 917 CHD and 8622 strokes) in EPIC-CVD,
                      Million Veteran Program, and UK Biobank.Results: There were
                      U-shaped observational associations of creatinine-based eGFR
                      with CHD and stroke, with higher risk in participants with
                      eGFR values <60 or >105 mL·min-1·1.73 m-2, compared with
                      those with eGFR between 60 and 105 mL·min-1·1.73 m-2.
                      Mendelian randomization analyses for CHD showed an
                      association among participants with eGFR <60 mL·min-1·1.73
                      m-2, with a $14\%$ $(95\%$ CI, $3\%-27\%)$ higher CHD risk
                      per 5 mL·min-1·1.73 m-2 lower genetically predicted eGFR,
                      but not for those with eGFR >105 mL·min-1·1.73 m-2.
                      Results were not materially different after adjustment for
                      factors associated with the eGFR genetic risk score, such as
                      lipoprotein(a), triglycerides, hemoglobin A1c, and blood
                      pressure. Mendelian randomization results for stroke were
                      nonsignificant but broadly similar to those for
                      CHD.Conclusions: In people without manifest cardiovascular
                      disease or diabetes, mild-to-moderate kidney dysfunction is
                      causally related to risk of CHD, highlighting the potential
                      value of preventive approaches that preserve and modulate
                      kidney function.},
      cin          = {C070 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C020-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36314129},
      doi          = {10.1161/CIRCULATIONAHA.122.060700},
      url          = {https://inrepo02.dkfz.de/record/182352},
}