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Serum uric acid is associated with increased risk of posttransplantation diabetes in kidney transplant recipients: a prospective cohort study
被引:5
|作者:
Sotomayor, Camilo G.
[1
]
Oskooei, Sara Sokooti
[1
]
Bustos, Nicolas I.
[2
]
Nolte, Ilja M.
[3
]
Gomes-Neto, Antonio W.
[1
]
Erazo, Marcia
[2
]
Gormaz, Juan G.
[2
]
Berger, Stefan P.
[1
]
Navis, Gerjan J.
[1
]
Rodrigo, Ramon
[2
]
Dullaart, Robin P. F.
[4
]
Bakker, Stephan J. L.
[1
]
机构:
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, Groningen, Netherlands
[2] Univ Chile, Fac Med, Santiago, Chile
[3] Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands
[4] Univ Groningen, Univ Med Ctr Groningen, Dept Endocrinol, Groningen, Netherlands
来源:
关键词:
Uric acid;
Posttransplantation diabetes;
Kidney transplantation;
Inflammation;
Oxidative stress;
Metabolic syndrome;
ENDOTHELIAL DYSFUNCTION;
RENAL-TRANSPLANTATION;
COMPETING RISKS;
GLUCOSE-UPTAKE;
HYPERURICEMIA;
MELLITUS;
SURVIVAL;
INFLAMMATION;
RECOMMENDATIONS;
METABOLISM;
D O I:
10.1016/j.metabol.2020.154465
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Background: Serum uric acid (SUA) is associated with fasting glucose in healthy subjects, and prospective epidemological studies have shown that elevated SUA is associated with increased risk of type 2 diabetes. Whether SUA is independently associated with higher risk of posttransplantation diabetes mellitus (PTDM) in kidney transplant recipients (KTR) remains unknown. Methods: We performed a longitudinal cohort study of 524 adult KTR with a functioning graft >= 1-year, recruited at a university setting (2008-2011). Multivariable-adjusted Cox proportional-hazards regression analyses were performed to assess the association between time-updated SUA and risk of PTDM (defined according the American Diabetes Association's diagnostic criteria). Results: Mean (SD) SUA was 0.43 (0.11) mmol/L at baseline. During 5.3 (IQR, 4.1-6.0) years of follow-up, 52 (10%) KTR developed PTDM. In univariate prospective analyses, SUA was associated with increased risk of PTDM (HR 1.75, 95% CI 1.36-2.26 per 1-SD increment; P < 0.001). This finding remained materially unchanged after adjustment for components of the metabolic syndrome, lifestyle, estimated glomerular filtration rate, immunosuppressive therapy, cytomegalovirus and hepatitis C virus infection (HR 1.89, 95% CI 1.32-2.70; P = 0.001). These findings were consistent in categorical analyses, and robust in sensitivity analyses without outliers. Conclusions: In KTR, higher SUA levels are strongly and independently associated with increased risk of PTDM. Our findings are in agreement with accumulating evidence supporting SUA as novel independent risk marker for type 2 diabetes, and extend the evidence, for the first time, to the clinical setting of outpatient KTR. (C) 2020 The Author(s). Published by Elsevier Inc.
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