Ryan J J, Beynon H L, Rees A J, Cassidy M J
Department of Medicine, Royal Postgraduate Medical School, London, England, United Kingdom.
Kidney Int Suppl. 1993 Jun;41:S226-9.
Cellular release of cytokines may be responsible for certain complications of extracorporeal dialysis including the increased susceptibility to infection found in dialysis patients. In order to study this further, we have evaluated the in vitro production of tumor necrosis factor (TNF) by peripheral blood monocytes (PBMC) to stimulation by lipopolysaccharide (LPS) from dialysis patients with end-stage renal failure (ESRF). The patients were subdivided into two groups according to the type of dialysis; those undergoing hemodialysis (HD) (N = 12) and those performing continuous ambulatory peritoneal dialysis (CAPD) (N = 9). Results were compared with those of controls taken from healthy laboratory staff (N = 7). The experiments show that the secretion of TNF by PBMC's in response to LPS is significantly augmented in patients undergoing HD when compared to those on CAPD (81.3 +/- 38.7 U/ml vs. 18.2 + 13.3 U/ml, mean +/- SD, P < 0.001); and controls (81.3 +/- 38.7 U/ml vs. 18.1 +/- 6.6 U/ml, P < 0.001). There was no significant difference between the CAPD group and controls. In vitro monocyte production of TNF fell following a single HD session (81.3 +/- 38.7 U/ml before HD and 50.5 +/- 28.7 U/ml after HD, P < 0.05). We conclude from this study that TNF release from PBMC's in vitro is augmented in patients with chronic renal failure receiving chronic HD but not in a similar group receiving CAPD. Interestingly, TNF release from monocytes collected immediately following a dialysis was suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)
细胞因子的细胞释放可能是体外透析某些并发症的原因,包括透析患者中发现的感染易感性增加。为了进一步研究这一点,我们评估了终末期肾衰竭(ESRF)透析患者外周血单核细胞(PBMC)对脂多糖(LPS)刺激的肿瘤坏死因子(TNF)体外产生情况。根据透析类型将患者分为两组;进行血液透析(HD)的患者(N = 12)和进行持续性非卧床腹膜透析(CAPD)的患者(N = 9)。将结果与来自健康实验室工作人员的对照组(N = 7)进行比较。实验表明,与接受CAPD的患者相比,接受HD的患者中PBMC对LPS反应分泌的TNF显著增加(81.3±38.7 U/ml对18.2 + 13.3 U/ml,平均值±标准差,P < 0.001);与对照组相比(81.3±38.7 U/ml对18.1±6.6 U/ml,P < 0.001)。CAPD组与对照组之间无显著差异。单次HD治疗后,体外单核细胞TNF产生量下降(HD前81.3±38.7 U/ml,HD后50.5±28.7 U/ml,P < 0.05)。我们从这项研究得出结论,慢性肾衰竭接受慢性HD的患者体外PBMC释放的TNF增加,但接受CAPD的类似组中未增加。有趣的是,透析后立即收集的单核细胞释放的TNF受到抑制。(摘要截断于250字)