In-vitro growth patterns of bone marrow erythroid progenitors from patients with post-renal transplant erythrocytosis.

ies suggest that in these cases erythrocytosis may be caused by defective regulation of erythroid progenitor Background. Erythrocytosis is relatively common after renal transplantation and is associated with a higher proliferation, possibly due to particular cellular interactions or the eVect of cyclosporin on erythropoiesis. risk of thromboembolism. Its aetiology is unclear and there is still debate about the most frequently suggested causes. The culture in vitro of erythroid progenitors is Key words: erythrocytosis; erythroid progenitors; regarded as a useful tool for the diVerential diagnosis erythropoietin; renal transplantation of patients with unclear erythrocytosis. We studied the growth in vitro of bone marrow erythroid progenitors from renal transplant patients with erythrocytosis and controls without erythrocytosis Subjects and methods. Thirteen renal transplant Introduction patients with erythrocytosis and 12 normocythaemic renal transplant controls were studied. The clinical Successful renal transplantation usually corrects renal characteristics of these patients were evaluated and anaemia within 8 to 10 weeks [1]. However, the serum erythropoietin ( Epo) and ferritin levels were haematocrit continues to rise in some patients even determined. Bone marrow erythroid progenitors were after complete correction of anaemia, resulting in postcultured both with and without the addition of Epo to transplant erythrocytosis (PTE ) with significant morthe medium. bidity due to thromboembolism. The published incidResults. Samples from six polycythaemic patients and ence rates for PTE are between 6.5 and 38.4% [2‐7]. seven controls did not grow spontaneously in the The cause of PTE is unclear. The haematocrit may absence of exogenous Epo. Three cases of post- increase because of a reduction in plasma volume. This transplant erythrocytosis and five controls produced is known as spurious erythrocytosis [8], and it responds CFU-E, but not BFU-E. A few CFU-E and BFU-E to increased salt and water intake. The haematocrit grew spontaneously in samples from four polycy- may also increase because of an increase in red blood thaemic patients but not in samples from the controls. cell (RBC ) mass. This is true erythrocytosis. The two Addition of 1 unit per millilitre Epo caused similar situations can be distinguished only by isotopic measincreases in the number of colonies in both polycy- urements of RBC mass and plasma volume [4]. Many thaemic patients and controls. Of the nine patients aetiological factors have been linked to true PTE, eligible for follow-up, all four with spontaneous growth including acute and chronic rejection [9], transplant of BFU-E had transient erythrocytosis and four of the artery stenosis [10], increased Epo formation by the five patients with no spontaneous growth or spontan- native kidneys [11,12], smoking and diabetes [3,13], eous growth of CFU-E only had persistent erythro- and the type and dose of immunosuppressive therapy cytosis requiring treatment with ACE inhibitors. used [6 ]. Treatment with rHuEpo prior to transplantaConclusions. Pathophysiology of post-transplant ery- tion may protect against PTE [14]. None of these throcytosis is heterogeneous. In one-third of the underlying factors is enough in itself to account compatients, there was unexpected, spontaneous and tran- pletely for the pathogenesis of PTE [7]. Culture of sient growth of BFU-E which was not predictive of erythroid progenitors in vitro is useful for the diVerenpermanent erythrocytosis. The results of stem-cell stud- tial diagnosis of patients with unclear erythrocytosis [15]. We have therefore studied the growth in vitro of