Angiogenesis and mechanisms of vascular repair are currently gaining a lot of attention as new avenues for cardiovascular and renal therapy. The present concept is that cells participating in repair can be either vessel-wall–derived or circulation-derived. In vitro experiments1-4 showed that human CD34 cells were able to differentiate into endothelial cells, suggesting potential involvement of stem cells in processes such as angiogenesis and vascular repair. In agreement, labeled CD34 cells have been shown to be incorporated into the vessel wall in experimental models of neovascularization. Participation of circulating endothelial cells in human vascular repair was recently shown by Lagaaij et al5 in kidneys. They identified acceptor endothelial cells in allografted donor kidneys. The number of acceptor endothelial cells was increased after vascular rejection, suggesting a role of these cells in vascular repair. The source of these circulating endothelial cells, however, still remains unclear. Here we present evidence that human endothelial injury repair involves bone-marrow–derived re-endothelialization.

A 28-year-old woman suffering from malignant hypertension was admitted to our hospital for a renal biopsy. Six months earlier, she underwent a bone marrow transplantation because of a relapsing acute myeloid leukemia M2 (AML-M2). After total body irradiation (2 consecutive 600 cGy doses) and cyclophosphamide conditioning (2 days at 60 mg/kg), she received T-cell–depleted