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GWAS Study

The genetic architecture of membranous nephropathy and its potential to improve non-invasive diagnosis.

Xie J, Liu L, Mladkova N et al.

32231244 PubMed ID
GWAS Study Type
12820 Participants
211 Views
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

XJ
Xie J
LL
Liu L
MN
Mladkova N
LY
Li Y
RH
Ren H
WW
Wang W
CZ
Cui Z
LL
Lin L
HX
Hu X
YX
Yu X
XJ
Xu J
LG
Liu G
CY
Caliskan Y
SC
Sidore C
BO
Balderes O
RR
Rosen RJ
BM
Bodria M
ZF
Zanoni F
ZJ
Zhang JY
KP
Krithivasan P
MK
Mehl K
MM
Marasa M
KA
Khan A
OF
Ozay F
CP
Canetta PA
BA
Bomback AS
AG
Appel GB
SS
Sanna-Cherchi S
SM
Sampson MG
ML
Mariani LH
PA
Perkowska-Ptasinska A
DM
Durlik M
MK
Mucha K
MB
Moszczuk B
FB
Foroncewicz B
PL
Pączek L
HI
Habura I
AE
Ars E
BJ
Ballarin J
ML
Mani LY
VB
Vogt B
OS
Ozturk S
YA
Yildiz A
SN
Seyahi N
AH
Arikan H
KM
Koc M
BT
Basturk T
KG
Karahan G
AS
Akgul SU
SM
Sever MS
ZD
Zhang D
SD
Santoro D
BM
Bonomini M
LF
Londrino F
GL
Gesualdo L
RJ
Reiterova J
TV
Tesar V
IC
Izzi C
SS
Savoldi S
SD
Spotti D
MC
Marcantoni C
MP
Messa P
GM
Galliani M
RD
Roccatello D
GS
Granata S
ZG
Zaza G
LF
Lugani F
GG
Ghiggeri G
PI
Pisani I
AL
Allegri L
SB
Sprangers B
PJ
Park JH
CB
Cho B
KY
Kim YS
KD
Kim DK
SH
Suzuki H
AA
Amoroso A
CD
Cattran DC
FF
Fervenza FC
PA
Pani A
HP
Hamilton P
HS
Harris S
GS
Gupta S
CC
Cheshire C
DS
Dufek S
IN
Issler N
PR
Pepper RJ
CJ
Connolly J
PS
Powis S
BD
Bockenhauer D
SH
Stanescu HC
AN
Ashman N
LR
Loos RJF
KE
Kenny EE
WM
Wuttke M
EK
Eckardt KU
KA
Köttgen A
HJ
Hofstra JM
CM
Coenen MJH
KL
Kiemeney LA
AS
Akilesh S
KM
Kretzler M
BL
Beck LH
SB
Stengel B
DH
Debiec H
RP
Ronco P
WJ
Wetzels JFM
ZM
Zoledziewska M
CF
Cucca F
II
Ionita-Laza I
LH
Lee H
HE
Hoxha E
SR
Stahl RAK
BP
Brenchley P
SF
Scolari F
ZM
Zhao MH
GA
Gharavi AG
KR
Kleta R
CN
Chen N
KK
Kiryluk K
Chapter II

Abstract

Summary of the research findings

Membranous Nephropathy (MN) is a rare autoimmune cause of kidney failure. Here we report a genome-wide association study (GWAS) for primary MN in 3,782 cases and 9,038 controls of East Asian and European ancestries. We discover two previously unreported loci, NFKB1 (rs230540, OR = 1.25, P = 3.4 × 10-12) and IRF4 (rs9405192, OR = 1.29, P = 1.4 × 10-14), fine-map the PLA2R1 locus (rs17831251, OR = 2.25, P = 4.7 × 10-103) and report ancestry-specific effects of three classical HLA alleles: DRB1*1501 in East Asians (OR = 3.81, P = 2.0 × 10-49), DQA1*0501 in Europeans (OR = 2.88, P = 5.7 × 10-93), and DRB1*0301 in both ethnicities (OR = 3.50, P = 9.2 × 10-23 and OR = 3.39, P = 5.2 × 10-82, respectively). GWAS loci explain 32% of disease risk in East Asians and 25% in Europeans, and correctly re-classify 20-37% of the cases in validation cohorts that are antibody-negative by the serum anti-PLA2R ELISA diagnostic test. Our findings highlight an unusual genetic architecture of MN, with four loci and their interactions accounting for nearly one-third of the disease risk.

2,150 European ancestry cases, 5,829 European ancestry controls, 1,612 East Asian ancestry cases, 1,970 East Asian ancestry controls

Chapter III

Study Statistics

Key metrics and study information

12820
Total Participants
GWAS
Study Type
Yes
Replicated
826 Chinese ancestry cases, 1,239 Chinese ancestry controls
Replication Participants
East Asian, European
Ancestry
China, Japan, Republic of Korea, Turkey, Germany, Italy, Poland, U.K., U.S.
Recruitment Country
Chapter IV

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