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GWAS Study

The Genetic Landscape of Renal Complications in Type 1 Diabetes.

Sandholm N, Van Zuydam N, Ahlqvist E et al.

27647854 PubMed ID
GWAS Study Type
11665 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

SN
Sandholm N
VZ
Van Zuydam N
AE
Ahlqvist E
JT
Juliusdottir T
DH
Deshmukh HA
RN
Rayner NW
DC
Di Camillo B
FC
Forsblom C
FJ
Fadista J
ZD
Ziemek D
SR
Salem RM
HL
Hiraki LT
PM
Pezzolesi M
TD
Trégouët D
DE
Dahlström E
VE
Valo E
ON
Oskolkov N
LC
Ladenvall C
MM
Marcovecchio ML
CJ
Cooper J
SF
Sambo F
MA
Malovini A
MM
Manfrini M
MA
McKnight AJ
LM
Lajer M
HV
Harjutsalo V
GD
Gordin D
PM
Parkkonen M
TJ
Tuomilehto J
LV
Lyssenko V
MP
McKeigue PM
RS
Rich SS
BM
Brosnan MJ
FE
Fauman E
BR
Bellazzi R
RP
Rossing P
HS
Hadjadj S
KA
Krolewski A
PA
Paterson AD
FJ
Florez JC
HJ
Hirschhorn JN
MA
Maxwell AP
DD
Dunger D
CC
Cobelli C
CH
Colhoun HM
GL
Groop L
MM
McCarthy MI
GP
Groop PH
Chapter II

Abstract

Summary of the research findings

Diabetes is the leading cause of ESRD. Despite evidence for a substantial heritability of diabetic kidney disease, efforts to identify genetic susceptibility variants have had limited success. We extended previous efforts in three dimensions, examining a more comprehensive set of genetic variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross-sectional diabetic kidney disease phenotypes. In 2843 subjects, we estimated that the heritability of diabetic kidney disease was 35% (P=6.4×10-3). Genome-wide association analysis and replication in 12,540 individuals identified no single variants reaching stringent levels of significance and, despite excellent power, provided little independent confirmation of previously published associated variants. Whole-exome sequencing in 997 subjects failed to identify any large-effect coding alleles of lower frequency influencing the risk of diabetic kidney disease. However, sets of alleles increasing body mass index (P=2.2×10-5) and the risk of type 2 diabetes (P=6.1×10-4) associated with the risk of diabetic kidney disease. We also found genome-wide genetic correlation between diabetic kidney disease and failure at smoking cessation (P=1.1×10-4). Pathway analysis implicated ascorbate and aldarate metabolism (P=9.0×10-6), and pentose and glucuronate interconversions (P=3.0×10-6) in pathogenesis of diabetic kidney disease. These data provide further evidence for the role of genetic factors influencing diabetic kidney disease in those with type 1 diabetes and highlight some key pathways that may be responsible. Altogether these results reveal important biology behind the major cause of kidney disease.

729 European ancestry cases, 84 cases, 3,290 European ancestry controls, 705 controls

Chapter III

Study Statistics

Key metrics and study information

11665
Total Participants
GWAS
Study Type
Yes
Replicated
94 European ancestry cases, 964 cases, 993 European ancestry controls, 4806 controls
Replication Participants
European
Ancestry
Finland, Poland, U.K., Austria, Sweden
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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