Renalase and endothelial dysfunction in heart transplant recipients.

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). 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. 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. 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.