Elsevier

Transplantation Proceedings

Volume 45, Issue 1, January–February 2013, Pages 394-396
Transplantation Proceedings

Thoracic transplantation
Complications
Renalase and Endothelial Dysfunction in Heart Transplant Recipients

https://doi.org/10.1016/j.transproceed.2012.02.042Get rights and content

Abstract

Introduction

Renalase, an enzyme that cetabolyzes catecholamines, such as circulating adrenaline and noradrenaline, is released by the human kidney to regulate blood pressure. In solid organ transplant recipients endothelial dysfunction is often present. The aim of our study was to assess correlations among renalase, blood pressure, endothelial injury markers, and kidney function in 130 prevalent heart allograft recipients (OHT).

Methods

Complete blood counts, urea, serum lipids, fasting glucose and creatinine were measured using standard laboratory methods in the hospital central laboratory. We assessed markers of endothelial function/injury: vWF (von Willebrand factor), inflammation: hsCRP, interleukin (IL)-6, TRAIL (tumor necrosis factor related apoptosis-inducing ligand), TWEAK (tumor necrosis factor-like weak inducer of apoptosis) and midkine renalase using commercially available kits.

Results

The mean serum renalase among OHT was significantly higher compared with a control group (P < .001). Among heart transplant recipients renalase correlated weakly (P < .05) with time after transplantation and TRAIL; moderately (P < .01), with ejection fraction and age; and strongly, with kidney function, IL-6, vWF, midkine, and New York Heart Association class (P < .05). Multiple regression analysis revealed renalase values to be 70% predicted by serum creatinine measurements.

Conclusion

Impaired kidney function was strongly associated with endothelial damage and inflammation. Renalase, which was highly elevated among heart transplant recipients, was predominantly dependent on renal function, which deteriorated with time after transplantation and in correlation with age.

Section snippets

Patients and Methods

The 130 patients who had undergone their first OHT in a single institution, are described in Table 1 All of them were transplanted using the Shumway-Cooley-Brock technique. Prior to OHT the serum creatinine in all patients was below 162 μmol/L (less than 1.8 mg/dL). In 20% of them induction therapy included antithymocyte globulin (1.25 mg/kg/day) administered for 3 consecutive days. Lymphocyte subpopulations were monitored during this time by flow cytometry. The immunosuppressive regimen of

Results

Clinical and biochemical data of heart allograft recipients are shown in Table 1 Their mean serum renalase values were significantly higher compared with the control group: 8.41 ± 5.47 μg/mL versus 3.86 ± 0.73 μg/mL respectively (P < .001). Renalase correlated weakly with time after transplantation (r = 0.22, P < .05) and TRAIL (r = −.21, P < .05); moderately with age (r = .25, P < .01), ejection fraction (r = −.26, P < .01); and strongly with erythrocyte count (r = −0.42, P < .0001),

Discussion

We have shown renalase to be related, on univariate analysis to markers of endothelial cell injury and inflammation. However, the only predictor of renalase was serum creatinine on multiple regression analysis. Renalase was significantly higher among heart transplant recipients compared with healthy volunteers. In our previous study we observed clinically significant CKD (estimated GFR < 60 mL/min/1.73 m2) among 62.57% and 61.96% of heart allograft recipients according to MDRD and CKD-EPI

References (15)

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