Hyperuricemia Predicts Kidney Disease Progression After Acute Allograft Dysfunction

Abstract Background Hyperuricemia is associated with the development of new cardiovascular events and chronic allograft nephropathy in patients with decreased allograft function. This study investigates whether hyperuricemia in kidney transplant recipients should be considered as an independent pred...

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Veröffentlicht in:Transplantation proceedings 2014, Vol.46 (2), p.499-504
Hauptverfasser: Weng, S.-C, Shu, K.-H, Wu, M.-J, Cheng, C.-H, Chen, C.-H, Yu, T.-M, Chuang, Y.-W, Huang, S.-T, Tarng, D.-C
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Sprache:eng
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Zusammenfassung:Abstract Background Hyperuricemia is associated with the development of new cardiovascular events and chronic allograft nephropathy in patients with decreased allograft function. This study investigates whether hyperuricemia in kidney transplant recipients should be considered as an independent predictor of kidney disease progression after acute allograft dysfunction. Methods Between September 1, 2010, and December 31, 2012, 124 patients who underwent kidney graft biopsy for acute allograft dysfunction were enrolled. Participants were divided into 2 groups: A hyperuricemi c group (n = 57) and a normouricemic group (n = 67). The mean serum uric acid (UA) level was obtained by averaging all measurements, once per month for 3 months, before the study began. Clinical and laboratory data were collected. We investigated the role of hyperuricemia on the composite end point (CEP) of doubling of serum creatinine and graft failure by using Cox regression and Kaplan-Meier plots. Results Over a mean follow-up of 14.27 months, the hyperuricemic group had a poor cumulative survival and easily reached the CEP of doubling of serum creatinine and graft failure ( P  = .025) with a first-year cumulative incidence of 29.84% and a second-year cumulative incidence of 35.09%. Cox regression models revealed that age at biopsy (unadjusted hazard ratio [HR], 1.03; 95% CI, 1.00–1.06), hyperuricemia (HR, 2.24; 95% CI, 1.13–4.46), and interstitial fibrosis and tubular atrophy (IF/TA), including 
ISSN:0041-1345
1873-2623
DOI:10.1016/j.transproceed.2013.09.040