INVITRO PRODUCTION OF TUMOR-NECROSIS-FACTOR BY MONOCYTES CULTURED FROM DIALYSIS PATIENTS

Citation
Jj. Ryan et al., INVITRO PRODUCTION OF TUMOR-NECROSIS-FACTOR BY MONOCYTES CULTURED FROM DIALYSIS PATIENTS, Kidney international, 43, 1993, pp. 226-229
Citations number
20
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00852538
Volume
43
Year of publication
1993
Supplement
41
Pages
226 - 229
Database
ISI
SICI code
0085-2538(1993)43:<226:IPOTBM>2.0.ZU;2-C
Abstract
Cellular release of cytokines may be responsible for certain complicat ions of extracorporeal dialysis including the increased susceptibility to infection found in dialysis patients. In order to study this furth er, we have evaluated the in vitro production of tumor necrosis factor (TNF) by peripheral blood monocyles (PBMC) to stimulation by lipopoly saccharide (LPS) from dialysis patients with end-stage renal failure ( ESRF). The patients were subdivided into two groups according to the t ype 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 labora tory staff (N = 7). The experiments show that the secretion of TNF by PBMC's in response to LPS is significantly augmented in patients under going 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/m l vs. 18.1 +/- 0.6 U/ml, P < 0.001). There was no significant differen ce between the CAPD group and controls. In vitro MonoCyte production o f 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 stu dy 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 i mmediately following a dialysis was suppressed. We suggest that HD rat her than uremia itself up-regulates monocyte secretion of TNF in vitro and that this is not an immediate response to activation by membrane polymer.