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Hyperuricemia Predicts Kidney Disease Progression After Acute Allograft Dysfunction
Authors:S.-C. Weng  K.-H. Shu  M.-J. Wu  C.-H. Cheng  C.-H. Chen  T.-M. Yu  Y.-W. Chuang  S.-T. Huang  D.-C. Tarng
Affiliation:1. Center for Geriatrics and Gerontology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung;2. Division of Nephrology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung;3. Institute of Clinical Medicine, National Yang-Ming University, Taipei;4. School of Medicine, Chung Shan Medical University, Taichung;5. School of Medicine, College of Medicine, China Medical University, Taichung;6. Department of Biotechnology, Hung Kuang University, Taichung;g Department and Institute of Physiology, National Yang-Ming University, Taipei;h Division of Nephrology, Department of Medicine, and Immunology Research Center, Taipei Veterans General Hospital, Taipei, Taiwan
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 hyperuricemic 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 <25% of parenchyma affected (HR, 3.71; 95% CI, 1.34–10.31) and ≥25% of parenchyma affected (HR, 5.10; 95% CI, 1.83–14.19), were highly associated with poor outcome. After adjusting different variables, hyperuricemia and IF/TA were still significant.

Conclusion

Persistently high serum UA and IF/TA both contribute to the risk of kidney disease progression after acute allograft dysfunction.
Keywords:
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