Erythroid Progenitor Growth in Erythrocytosic Transplanted Patients

Abstract

In 55 patients who underwent renal transplantation, erythrocytosis (E) was observed in 6. In all patients, the growth of erythroid progenitors [burst-forming unit erythroid (BFU-e)], using mononuclear blood cells, was evaluated in in vitro cultures. The results showed a significant increase of serum erythropoietin (s-Ep) in erythrocytosis and in nonerythrocytosis patients with a subsequent decrease when hematocrit (Hct) and hemoglobin (Hb) reached high levels, showing a recovery of a feedback control system. Notwithstanding the diminution of s-Ep, six patients demonstrated further progressive rise of the Hct and Hb to a final state of E. The in vitro BFU-e cultures from these patients showed a noticeable sensitivity to progressively reduced doses of Ep and also the capacity to develop a few colonies when the medium was Ep-free. These results were not verified using peripheral blood depleted of monocyte and/or T lymphocyte cells. Therefore, in transplanted patients with erythrocytosis, it is possible that particular cellular interactions stimulate an early hyperproliferation of BFU-e with a greater Ep sensitivity and at least partly the capacity to grow also in the absence of Ep.

Post‐transplantation erythrocytosis in kidney transplant recipients—A retrospective cohort study

“…Various levels of erythropoietin were found in PTE patients, 8,9 and PTE has been shown to be related to increased sensitivity to erythropoietin. 10,11 Another contributing factor is the renin-angiotensin System (RAS). Angiotensin1 receptor was found to be augmented in PTE patients and associated with proliferation of erythroid progenitors.…”