Department of Internal Medicine, University of Messina, Messina - Italy.
J Nephrol. 2010 May-Jun;23(3):328-34.
End stage renal disease (ESRD) is associated with a high incidence of cardiovascular disease and cancer. Patients undergoing hemodialysis show a reduced number and an impaired function of endothelial progenitor cells (EPCs), which in physiological conditions contribute to repair the vascular damage. In patients with ESRD, massive oxidative genome damage has been demonstrated but the role of HD in causing it is still a controversial issue. The aim of our study was to analyze the effects of a single HD session on the number of cells marked with CD34 (including sub-type cells known to be EPCs); we then evaluated the genomic damage in these cells using COMET assay.
We quantified CD34(+) cells in blood samples in 30 patients in hemodiafiltration treatment for 3.5 to 4 hours 3 times/week and in 30 healthy volunteers. In HD patients, blood samples were drawn at different time intervals: start of dialysis (T(0)), at the end of the treatment (T(end)) and 24 hours afterwards in the interdialytic day (T(inter)). Staining and analysis was performed using the ISHAGE (International Society of Hematotherapy and Graft Engineering) guidelines. EPCs count was conducted using a multiparameter flow cytometric lyse no-wash method. Genomic damage was evaluated by Comet assay.
The number of CD34(+) cells in the HD patients at the beginning of the dialysis session (T(0)) was significantly lower than in healthy controls. HD patients showed a significant increase in CD34 number at the end of the session (T(end)) with respect to T(0). In the interdialytic period (T(int)), the number of CD34(+) cells was significantly reduced with respect to T(end). COMET assay performed on CD34(+) cells showed a higher basal level of genomic damage in HD patients than in controls; it increased in a statistically significant manner after the hemodialysis session, while in the interdialytic period it came back to T(0) level.
Uremic status is characterized by lower levels of circulating EPCs, which increase after a single session of HD together with genomic damage to the CD34(+) cells.
终末期肾病（ESRD）与心血管疾病和癌症的发病率高有关。接受血液透析的患者表现出内皮祖细胞（EPC）数量减少和功能受损，而在生理条件下，EPC 有助于修复血管损伤。在 ESRD 患者中，大量氧化基因组损伤已得到证实，但 HD 导致这种损伤的作用仍是一个有争议的问题。我们的研究目的是分析单次血液透析治疗对标记有 CD34 的细胞数量（包括已知为 EPC 的亚群细胞）的影响；然后使用彗星试验评估这些细胞的基因组损伤。
我们在每周 3 次、每次 3.5 至 4 小时的血液透析滤过治疗中，对 30 名血液透析患者和 30 名健康志愿者的血液样本进行了 CD34(+)细胞定量。在血液透析患者中，在不同时间点采集血液样本：透析开始时（T(0)）、治疗结束时（T(end)）和随后的无透析日（T(inter)）24 小时后。使用国际血液治疗和移植物工程学会（ISHAGE）指南进行染色和分析。使用多参数流式细胞术裂解无洗涤方法进行 EPC 计数。通过彗星试验评估基因组损伤。
透析开始时（T(0)）血液透析患者的 CD34(+)细胞数量明显低于健康对照组。血液透析患者在治疗结束时（T(end)）与 T(0)相比，CD34 数量显著增加。在无透析期（T(int)），与 T(end)相比，CD34(+)细胞数量明显减少。对 CD34(+)细胞进行彗星试验显示，血液透析患者的基因组损伤基础水平高于对照组；在血液透析治疗后呈统计学显著增加，而在无透析期则恢复到 T(0)水平。
尿毒症状态的特征是循环 EPC 水平较低，单次血液透析后 EPC 水平升高，同时 CD34(+)细胞的基因组损伤增加。
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