In-vitro growth patterns of bone marrow erythroid progenitors from patients with post-renal transplant erythrocytosis |
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Authors: | Hestin D; Gregoire M; Mayeux D; Mertes P; Lakomsky D; Kessler M |
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Institution: | Department of Nephrology, Laboratory of Genetics, Department of Biostatistics, Hormonal and Metabolic Function laboratory, Laboratory of Haematology, CHU de Nancy, 54500 Vandoeuvre les Nancy, France; Corresponding author |
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Abstract: | Background: Erythrocytosis is relatively common after
renal transplantation and is associated with a higher 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 regarded as a useful tool for
the differential diagnosis of patients with unclear erythrocytosis. We
studied the growth in vitro of bone marrow erythroid
progenitor from renal transplant patients with erythrocytosis and controls
without erythrocytosis. Subjects and methods: Thirteen
renal transplant patients with erythrocytosis and 12 normocythaemic renal
transplant controls were studied. The clinical characteristics of these
patients were evaluated and serum erythropoietin (Epo) and ferritin levels
were determined. Bone marrow erythroid progenitors were cultured both with
and without the addition of Epo to the medium.
Results: Samples from six polycythaemic patients and
seven controls did not grow spontaneously in the absence of exogenous Epo.
Three cases of post-transplant erythrocytosis and five controls produced
CFU-E, but not BFU-3. A few CFU-E and BFU-E grew spontaneously in samples
from four polycythaemic patients but not in samples from the controls.
Addition of 1 unit per millilitre Epo caused similar increases in the
number of colonies in both polycythaemic patients and controls. Of the nine
patients eligible for follow-up, all four with spontaneous growth of BFU-E
had transient erythrocytosis and four of the five patients with no
spontaneous growth or spontaneous growth of CFU-E only had persistent
erythrocytosis requiring treatment with ACE inhibitors.
Conclusions: Pathophysiology of post-transplant
erythrocytes is heterogenous. In one-third of the patients, there was
unexpected, spontaneous and transient growth of BFU-E which was not
predictive of permanent erythrocytosis. The results of stem-cell studies
suggest that in these cases erythrocytosis may be caused by defective
regulation of erythroid progenitor proliferation, possibly due to
particular cellular interactions or the effect of cyclosporin on
erythropoiesis. |
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