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Abstract . A number of studies suggest that erythropoietin (Ep),  angiotensin II, and insulin-like growth factor (IGF-1) are involved in the  pathogenesis of posttransplantation erythrocytosis (PTE).  Angiotensin-converting enzyme inhibitors (ACEI) are the treatment of choice in  PTE, but their mechanism of action is unclear. It was shown previously that  ACEI added directly to cultures of erythroid precursors from patients with PTE  inhibit colony growth. In this report, the effect of ACEI on CD34+ erythroid  precursor apoptosis was studied, as were hematocrit (Hct), Ep, IGF-1, and  IGF-binding protein 3 (IGF-BP3) levels. Ten patients with PTE, 10 transplant  control patients, and 7 normal control subjects were studied. Peripheral blood  CD34+ cells were isolated, and apoptosis was assessed by annexin assay and DNA  laddering before and during ACEI therapy. At the same time, Hct, Ep, IGF-1,  and IGF-BP3 levels were measured. Baseline CD34+ cell number, CD34+ apoptosis,  Ep, IGF-1, and IGF-BP3 levels were the same between PTE and transplant control  subjects. ACEI therapy was associated with a striking increase in CD34+ cell  apoptosis and a decrease in Hct in both groups. In contrast to control  subjects, patients with PTE on ACEI showed a significant decrease in IGF-1  levels and a greater percentage decrease in Hct. In normal control subjects,  ACEI therapy was associated with a fall in Hct but no change in CD34+ cell  apoptosis. In PTE, ACEI-related increase in erythroid progenitor apoptosis may  partially explain the ACEI-associated decrease in Hct. However, it is not  clear that erythroid precursor apoptosis is related to changes in IGF-1 or  IGF-BP3.

journal of the american society of nephrology

Angiotensin-Converting Enzyme Inhibition Induces Apoptosis in Erythroid Precursors and Affects Insulin-Like Growth Factor-1 in Posttransplantation Erythrocytosis