Circulating endothelial cells are a novel marker of XXXX -induced endothelial damage.

@entity1 @entity14855 @entity9909 @entity205 @entity1140 @entity1011
Microvascular endothelial cells play a key role in transplant immunology. They are also important targets for calcineurin inhibitors. We recently demonstrated elevated numbers of circulating endothelial cells in renal transplant recipients with and without rejection in comparison with healthy controls. Because these @entity1 received either @entity205 or @entity1140 , we speculated that endothelial damage from calcineurin inhibitors might be responsible for these findings. In the present study, we tested the hypothesis that treatment with @entity14855 inhibitors leads to an increase in circulating endothelial cells. We studied 57 renal transplant recipients: 19 on a @entity9909 -free immunosuppressive regimen and 38 @entity1 on a standard immunosuppressive regimen, including @entity205 , and matched them for age and serum @entity1011 . Endothelial cells were isolated from peripheral blood with anti-CD-146-coated immunomagnetic Dynabeads and were counted by fluorescence microscopy. @entity1 with @entity205 therapy had elevated numbers of circulating endothelial cells (median 26, range 12 to 82 cells/mL) compared with healthy controls (median 6, range 0 to 82 cells/mL; P<0.001). @entity1 without @entity9909 treatment had significantly lower cell numbers (median 12, range 0 to 32 cells/mL; P<0.003) and were not significantly different from normal, untreated controls. In conclusion, renal transplant recipients who do not receive calcineurin inhibitors have significantly lower numbers of circulating endothelial cells than their age- and @entity1011 -matched counterparts who receive these drugs. We suggest that elevated numbers of circulating endothelial cells indicate damage from calcineurin inhibitors in renal transplant recipients and that circulating endothelial cells are a novel marker of endothelial damage.
