Apoptosis of Peripheral CD4(+) T-Lymphocytes in End-Stage Renal Disease Patients Under Hemodialysis and rhEPO Therapies

作者:Borges Ana; Borges Margarida; Fernandes Joao; Nascimento Henrique; Sameiro Faria Maria; Miranda Vasco; Reis Flavio; Belo Luis; Costa Elisio*; Santos Silva Alice
来源:Renal Failure, 2011, 33(2): 138-143.
DOI:10.3109/0886022X.2011.553300

摘要

End-stage renal disease (ESRD) under hemodialyses (HD) is related with a higher propensity to infections, essentially due to T-cell lymphopenia. We postulated that HD procedure affects CD4<SU++</SU T cells, especially by inducing apoptotic death and that recombinant human erythropoietin (rhEPO) therapy may also play an important role in the modulation of the immune system in these patients. T-cell phenotype and apoptosis of HD patients and healthy controls were evaluated by flow cytometry using anticoagulated whole-blood samples. In 12 HD patients, these parameters were also analyzed before and immediately after HD procedure. HD patients showed a decrease in total circulating CD3<SU++</SU lymphocytes, especially in CD4<SU++</SU T cells (0.747 +/-+/- 0.410 vs. 0.941 +/-+/- 0.216 xx 10<SU9</SU//L, p < 0.05), which could be a consequence of the higher proportion of CD3<SU++</SU and CD4<SU++</SU lymphocytes in the latest stage of apoptosis (or death) and of the higher proportion of apoptotic CD4<SU++</SU T cells observed in the patients immediately after HD procedure (2.91 +/-+/- 0.780 vs. 3.90 +/-+/- 1.96, p < 0.05). A positive and statistically significant correlation between CD3<SU++</SU and CD4<SU++</SU lymphocytes in latest stage of apoptosis (or death) with HD time was found (CD3<SU++</SU: r == 0.592, p < 0.01; CD4<SU++</SU: r == 0.501, p < 0.01). We also found a negative and significant correlation between weekly rhEPO doses and the number of CD4<SU++</SU T cells (r == --0.358, p < 0.05). In conclusion, HD procedure still contributes to the development of T-cell lymphopenia, at least in part, by apoptosis induction. It was also shown that rhEPO therapy is associated with the CD4<SU++</SU T-cell decline, possibly by immune modulation, eliminating atypical cells and helping to restore the CD4<SU++</SU T-cell subset.</.

  • 出版日期2011