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@ARTICLE{Teumer:144824,
author = {A. Teumer and Y. Li and S. Ghasemi and B. P. Prins and M.
Wuttke and T. Hermle and A. Giri and K. B. Sieber and C. Qiu
and H. Kirsten and A. Tin and A. Y. Chu and N. Bansal and M.
F. Feitosa and L. Wang and J.-F. Chai and M. Cocca and C.
Fuchsberger and M. Gorski and A. Hoppmann and K. Horn and M.
Li and J. Marten and D. Noce and T. Nutile and S. Sedaghat
and G. Sveinbjornsson and B. O. Tayo and P. J. van der Most
and Y. Xu and Z. Yu and L. Gerstner and J. Ärnlöv and S.
J. L. Bakker and D. Baptista and M. L. Biggs and E.
Boerwinkle and H. Brenner$^*$ and R. Burkhardt and R. J.
Carroll and M.-L. Chee and M.-L. Chee and M. Chen and C.-Y.
Cheng and J. P. Cook and J. Coresh and T. Corre and J.
Danesh and M. H. de Borst and A. De Grandi and R. de Mutsert
and A. P. J. de Vries and F. Degenhardt and K. Dittrich and
J. Divers and K.-U. Eckardt and G. Ehret and K. Endlich and
J. F. Felix and O. H. Franco and A. Franke and B. I.
Freedman and S. Freitag-Wolf and R. T. Gansevoort and V.
Giedraitis and M. Gögele and F. Grundner-Culemann and D. F.
Gudbjartsson and V. Gudnason and P. Hamet and T. B. Harris
and A. A. Hicks and H. Holm and V. H. X. Foo and S.-J. Hwang
and M. A. Ikram and E. Ingelsson and V. W. V. Jaddoe and J.
Jakobsdottir and N. S. Josyula and B. Jung and M. Kähönen
and C.-C. Khor and W. Kiess and W. Koenig and A. Körner and
P. Kovacs and H. Kramer and B. K. Krämer and F. Kronenberg
and L. A. Lange and C. D. Langefeld and J. J. Lee and T.
Lehtimäki and W. Lieb and S.-C. Lim and L. Lind and C. M.
Lindgren and J. Liu and M. Loeffler and L.-P. Lyytikäinen
and A. Mahajan and J. C. Maranville and D. Mascalzoni and B.
McMullen and C. Meisinger and T. Meitinger and K. Miliku and
D. O. Mook-Kanamori and M. Müller-Nurasyid and J. C.
Mychaleckyj and M. Nauck and K. Nikus and B. Ning and R.
Noordam and J. O. Connell and I. Olafsson and N. D. Palmer
and A. Peters and A. I. Podgornaia and B. Ponte and T.
Poulain and P. P. Pramstaller and T. J. Rabelink and L. M.
Raffield and D. F. Reilly and R. Rettig and M. Rheinberger
and K. M. Rice and F. Rivadeneira and H. Runz and K. A. Ryan
and C. Sabanayagam and K.-U. Saum$^*$ and B. Schöttker$^*$
and C. M. Shaffer and Y. Shi and A. V. Smith and K. Strauch
and M. Stumvoll and B. B. Sun and S. Szymczak and E.-S. Tai
and N. Y. Q. Tan and K. D. Taylor and A. Teren and Y.-C.
Tham and J. Thiery and C. H. L. Thio and H. Thomsen$^*$ and
U. Thorsteinsdottir and A. Tönjes and J. Tremblay and A. G.
Uitterlinden and P. van der Harst and N. Verweij and S.
Vogelezang and U. Völker and M. Waldenberger and C. Wang
and O. D. Wilson and C. Wong and T.-Y. Wong and Q. Yang and
M. Yasuda and S. Akilesh and M. Bochud and C. A. Böger and
O. Devuyst and T. L. Edwards and K. Ho and A. P. Morris and
A. Parsa and S. A. Pendergrass and B. M. Psaty and J. I.
Rotter and K. Stefansson and J. G. Wilson and K. Susztak and
H. Snieder and I. M. Heid and M. Scholz and A. S.
Butterworth and A. M. Hung and C. Pattaro and A. Köttgen},
title = {{G}enome-wide association meta-analyses and fine-mapping
elucidate pathways influencing albuminuria.},
journal = {Nature Communications},
volume = {10},
number = {1},
issn = {2041-1723},
address = {[London]},
publisher = {Nature Publishing Group UK},
reportid = {DKFZ-2019-02249},
pages = {4130},
year = {2019},
abstract = {Increased levels of the urinary albumin-to-creatinine ratio
(UACR) are associated with higher risk of kidney disease
progression and cardiovascular events, but underlying
mechanisms are incompletely understood. Here, we conduct
trans-ethnic (n = 564,257) and European-ancestry
specific meta-analyses of genome-wide association studies of
UACR, including ancestry- and diabetes-specific analyses,
and identify 68 UACR-associated loci. Genetic correlation
analyses and risk score associations in an independent
electronic medical records database (n = 192,868) reveal
connections with proteinuria, hyperlipidemia, gout, and
hypertension. Fine-mapping and trans-Omics analyses with
gene expression in 47 tissues and plasma protein levels
implicate genes potentially operating through differential
expression in kidney (including TGFB1, MUC1, PRKCI, and
OAF), and allow coupling of UACR associations to altered
plasma OAF concentrations. Knockdown of OAF and PRKCI
orthologs in Drosophila nephrocytes reduces albumin
endocytosis. Silencing fly PRKCI further impairs slit
diaphragm formation. These results generate a priority list
of genes and pathways for translational research to reduce
albuminuria.},
cin = {C070 / C120 / C050},
ddc = {500},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
I:(DE-He78)C050-20160331},
pnm = {313 - Cancer risk factors and prevention (POF3-313)},
pid = {G:(DE-HGF)POF3-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31511532},
pmc = {pmc:PMC6739370},
doi = {10.1038/s41467-019-11576-0},
url = {https://inrepo02.dkfz.de/record/144824},
}