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Medical Science Monitor Basic Research


eISSN: 2329-0358

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Serum Uric Acid and Arterial Function After Renal Transplantation

Frederic Bauer, Nikolaos Pagonas, Felix S. Seibert, Walter Zidek, Richard Viebahn, Nina Babel, Timm H. Westhoff

(Medical Department I, University Clinic Marienhospital Herne, Ruhr-University of Bochum, Herne, Germany)

Ann Transplant 2017; 22:431-439

DOI: 10.12659/AOT.901657

BACKGROUND: Hyperuricemia is associated with an increased risk of cardiovascular disease and chronic allograft nephropathy after renal transplantation. It has recently been demonstrated that treatment of asymptomatic hyperuricemia is associated with improved patient and graft survival; although, the underlying mechanisms remain elusive. The present study investigated the association of serum uric acid (SUA) and systemic arterial function after renal transplantation.
MATERIAL AND METHODS: In a cross-sectional study, arterial function was analyzed in 54 renal transplant recipients by means of pulse wave analysis. Different measurement techniques were combined providing data on pulse wave velocity, augmentation index, small and large artery elasticity, and total peripheral vascular resistance.
RESULTS: The prevalence of hyperuricemia was 87.0%, and 33.3% of renal transplant recipients received SUA lowering medication. The median SUA concentration was 7.4 mg/dL. There was no significant difference in all the aforementioned parameters in patients with a SUA <7.4 versus >7.4 mg/dL (p>0.05 each) and no significant differences between hyperuricemic patients with versus without SUA lowering medication. Linear regression analysis between SUA and both pulse wave velocity and augmentation index showed no significant association (p>0.05 each). This finding remained consistent after adjustment of data for age, time on dialysis, time since transplantation, and systolic blood (partial correlation analysis, p>0.05).
CONCLUSIONS: Neither the concentration of SUA nor the pharmacological treatment of hyperuricemia had measurable effects on arterial stiffness. Thus, the beneficial effects of SUA lowering treatment on patient and graft survival cannot be explained by direct effects on arterial function in the study population.

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