2010 - TTS International Congress


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Complications Cardiovascular

31.23 - The effect of hyperuricemia on endothelial biomarkers, renal function and cardiovascular disease in renal allograft recipients

Presenter: Maria, Boratynska, Wroclaw, Poland
Authors: Karbowska A., Boratynska M., Klinger M.

THE EFFECT OF HYPERURICEMIA ON ENDOTHELIAL BIOMARKERS, RENAL FUNCTION AND CARDIOVASCULAR DISEASE IN RENAL ALLOGRAFT RECIPIENTS

COMPLICATIONS - CARDIOVASCULAR

A. Karbowska, M. Boratynska, M. Klinger
Department Of Nephrology And Transplantation Medicine, Wroclaw Medical University, Wroclaw/POLAND

Body: Introduction
Epidemiological studies suggest, that hyperuricemia is a risk factor of hypertension, cardiovascular morbidity and kidney disease in general population. Hyperuricemia is common in renal transplant recipients treated with calcineurin inhibitors. It is unclear if an elevated uric acid has a causal role in progression of renal transplant injury or if it is a marker of renal injury. There has been no evidence provided that uric acid-lowering therapy may have beneficial effect on cardiovascular system or kidney allograft.
The aim of this study was to assess the influence of elevated serum uric acid level on biomarkers of endothelial activation and inflammation, renal function and cardiovascular disease in renal allograft recipients. Moreover, the influence of allopurinol and ACE inhibitors on renal function were estimated.
Patients and Methods
The study included 100 allograft recipients (age 46.3±13.3 years) with stable allograft function (eGFR>60 ml/min) treated with calcineurin inhibitor, MMF or azathioprine and corticosteroids. Exclusion criteria were gout, proteinuria, diabetes mellitus, obesity, and inflammatory diseases. The study was performed 34±12 months after transplantation. The patients were followed prospectively for 30 months.
Seventy patients had hyperuricemia (uric acid concentration 7.52±1.01 mg/dL) and 30 patients were normouricemic (5.48±0.92 mg/dL); control group. Treatment with allopurinol, and with ACE inhibitors was introduced in 22 hyperuricemic patients.
Concentrations of plasma resistin, soluble vascular cell adhesion molecule-1 (sVCAM-1), CRP were assessed in all patients. The biomarkers were repeated after 30 months of follow-up. Renal function and post-transplant cardiovascular disease were analyzed.
Results
No significant differences were noted between hyperuricemic and normouricemic group for demographics, dialysis and transplant related data.
Concentrations of the examined biomarkers were increased in the group with hyperuricemia compared with the control group: plasma resistin: 8.11±3.03 ng/mL vs 6.29±2.76 ng/mL (p<0.003); sVCAM-1: 1170±171 ng/mL vs 955±269 ng/mL (p<0.02). Serum uric acid level correlated with: CRP (r=0.2; P<004); sytolic and diastolic blood pressure (r=0.7; P<0.001); eGFR (r-0.5; P<0.001), cholesterol (r=0.2, P<0.01) and negatively with HDL cholesterol (r=-0.2; P<0.04).
After 30 months of treatment the hyperuricemic patients had slightly lower level of uric acid, sVCAM-1 was decreased, but resistin was increased. In the control group uric acid level did not change.
Impairiment of renal allograft function in hyperuricemic patients was comparable to normouricemic patients during 30 months follow-up; eGFR decreased from 66 to 52 ml/min vs. 76 to 55 ml/min.
There were 7 (10%) cardiovascular events in the hyperuricemic and 1 (3,3%) in the normouricemic group since transplant procedure (61 months). Two patients died (1 cancer in hyperuricemic group and 1 aortae dissection in control group). Nobody progressed to kidney allograft failure.
Conclusions
Hyperuricemia might injure systemic microvasculature through resistin and CD146 mechanisms. Hyperuricemia is a risk factor of arterial stiffness. We found, that moderate elevation of serum uric acid might not have a causal role in renal transplant injury during 30 months follow-up.

Disclosure: All authors have declared no conflicts of interest.


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