Angiogenic Activity in the Sera of Patients with Post-Kidney Transplant Erythrocytosis

Chokri Maktouf (1) , Soumaya Yaich (2) , Sabra Aloui (3) , Azza Bounemra (4) , Khaled Charfeddine (2) , Habib Skhiri (3) , Jamil Hachicha (2)

1 Institut Pasteur de Tunis
2 Hedi Chaker Hospital [Sfax]
3 Centre National de Transfusion Sanguine [Tunis]
4 HFB - CHU Fattouma Bourguiba [Monastir]

Post-kidney transplant erythrocytosis (PTE) is one of the hematological complications in the renal transplant patients. While its pathogenesis still remains to be elucidated completely, a number of therapies are available for the management of PTE. The aim of this prospective study was to investigate whether angiogenesis may be involved in the pathogenesis of post-transplant erythrocytosis by comparing its level with those of different classes of erythrocytosis [polycythemia vera (PV), idiopathic erythrocytosis and secondary erythrocytosis]. The angiogenic activity was evaluated by the assessment of the serum vascular endothelial growth factor (VEGF) levels, as one of circulating angiogenic factor, using a standardized enzyme-linked immunosorbent assay commercial kit in 13 PTE (2 F/11 M), in 75 untreated erythrocytosis non-transplant patients and in 21 healthy subjects controls. The results indicated that VEGF was overproduced in advanced and untreated PV patients and to a lesser degree in idiopathic erythrocytosis thus confirming an increased angiogenic activity. However, there is no evidence of increased angiogenesis in PTE and in secondary erythrocytosis. The absence of angiogenesis in PTE and its presence in PV is another argument that the pathogenesis of these two entities is different.

Domains: Life Sciences [q-bio]; Human health and pathology

Chokri Maktouf, Soumaya Yaich, Sabra Aloui, Azza Bounemra, Khaled Charfeddine, et al.. Angiogenic Activity in the Sera of Patients with Post-Kidney Transplant Erythrocytosis. Saudi Journal of Kidney Diseases and Transplantation , 2014, 25 (5), pp.1026-1029. ⟨10.4103/1319-2442.139905⟩. ⟨pasteur-02017903⟩