Lack of plasma interleukin-1β or tumor necrosis factor-α elevation during unfavorable hemodialysis conditions (original) (raw)
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Cellular & molecular immunology
Cytokines are essential mediators of immune response and inflammatory reactions. Patients with chronic renal failure (CRF) commonly present with abnormalities of immune function related with impaired kidney function and the accumulation of uremic toxins in addition to bioincompatibility of dialyzer membranes. During a hemodialysis (HD) session, cytokines are released mainly by monocytes activated by endotoxin-type compounds in dialyzer fluid, complement factors and direct contact with dialyzer membrane. The study included 15 CRF patients, aged 36.4 +/- 2.9 years, on regular HD maintenance therapy for mean 68 +/- 10 months and 15 healthy controls. It was designed to assess serum levels of a panel of inflammatory cytokines: IL-1beta, IL-2, IL-6, IL-8 and TNF-alpha in CRF patients on regular maintenance HD before, 20, 60 and 240 minutes of a single HD session in parallel with C-reactive protein (CRP) as an additional parameter. CRP concentration was increased in HD patients when compar...
The International Journal of Artificial Organs, 1992
Conflicting results have been published concerning the systemic induction of the cytokine tumor necrosis factor alpha (TNFα) during hemodialysis (HD). We therefore evaluated in vitro TNFα production in whole blood as well as in vivo variability of TNFα levels in patients on long-term HD. Whole blood was incubated at room temperature (RT) with or without exogenously added endotoxin (ET), and plasma-TNFα was measured after 5, 30, 120, 240, and 960 min by specific enzyme immunoassay. Additionally, plasma-TNFα before and after 120 and 240 min HD was studied longitudinally once a week over a period of 4 weeks in 36 patients on Cuprophan®(CU, n=23) or polysulfone-F60 (PSu, n=13) HD. Mean plasma TNFα levels in vitro rose from (mean) 8 pg/ml after 5 min to 12 pg/ml (120′) and 32 pg/ml (960′) even without ET addition, and to 18 pg/ml (after 120′) and 88 pg/ml (after 960′) when 0.1 μg/ml ET were added. Pre-dialytic as well as intradialytic TNFα levels in patients showed high intra-individual ...
In vivo induction of interleukin-1 during hemodialysis
Kidney International, 1989
In vivo induction of interleukin-1 during hemodialysis. In vivo induction of interleukin-1 (IL-i) production during hemodialysis was investigated by measuring IL-I activity in monocyte lysates from 59 patients undergoing long-term maintenance hemodialysis with complement activating and non-complement activating devices. In patients dialyzed with new hollow-fiber cuprophane dialyzers, predialytic (TO) monocyteassociated IL-i activity was 12.5 3.0 U/ml (mean SEM), a value that was higher than that found in normal individuals (2.85 0.85 U/mi; P <0.0025) and in non-dialyzed patients with chronic renal failure (0.95 0.85 U/ml, P < 0.0001). Cell-associated IL-i activity was consistently increased after five hours of dialysis with cuprophane membranes (42.4 5.5 U/mI, P < 0.0005). Systemic complement activation was demonstrated by the finding of increased plasma levels of C3adesArg antigen during dialysis. In patients dialyzed with high permeability polyacrylonitrile and polysulfone membranes, no intradialytic change in cellassociated IL-i and no complement activation occurred. However, the mean predialytic values of monocyte-associated IL-I in these patients (that is, 32.9 5.6 U/mI and 38 5.65 U/mI for the polyacrylonitrile and the polysulfone groups, respectively) were higher than the predialytic levels of cell-associated IL-I in the patients from the cuprophane group (P < 0.0025). Monocytes obtained at the beginning and five hours of dialysis from patients dialyzed with polyacryionitrile devices, and monocytes obtained at five hours but not at the beginning of dialysis from patients dialyzed with cuprophane membranes, spontaneously released extracellular IL-I after 24 hours of culture in serum free conditions. Neither polyacrylonitrile nor cuprophane differed in their capacity to stimulate monocytes that had adhered to the membrane, to produce IL-l in serum free cultures. These results indicate that IL-I is transiently generated during hemodialysis with complement activating membranes when C3aiC3adesArg and CsaiC5adesArg, which are known inducers of IL-i production, are generated in plasma. Noncomplement dependent factors, possibly LPS or fragments of LPS that often contaminate bicarbonate dialysates, may be responsible for chronic stimulation of IL-1 production in patients dialyzed with high permeability membranes.
Immune System Dysfunction and Inflammation in Hemodialysis Patients: Two Sides of the Same Coin
Journal of Clinical Medicine
Biocompatibility in hemodialysis (HD) has considerably improved in recent decades, but remains an open issue to be solved, appearing essential to reduce systemic inflammation and enhance patients’ clinical outcomes. Clotting prevention, reduction in complement and leukocyte activation, and improvement of antioxidant effect represent the main goals. This review aims to analyze the different pathways involved in HD patients, leading to immune system dysfunction and inflammation. In particular, we mostly review the evidence about thrombogenicity, which probably represents the most important characteristic of bio-incompatibility. Platelet activation is one of the first steps occurring in HD patients, determining several events causing chronic sub-clinical inflammation and immune dysfunction involvement. Moreover, oxidative stress processes, resulting from a loss of balance between pro-oxidant factors and antioxidant mechanisms, have been described, highlighting the link with inflammatio...
Inflammatory signals associated with hemodialysis
Kidney …, 2002
Inflammatory signals associated with hemodialysis. excretion of cytokines, and certain co-morbid condition Background. Inflammation is highly prevalent in chronic he-[6-8]. The hemodialysis procedure has also been sugmodialysis patients. Because hemodialysis involves the contact gested as a potential source of inflammation in chronic of blood with "foreign" surfaces, and the documented activahemodialysis patients. tion of several humoral and cellular pathways during the pro-Several reports have documented the catabolic effects cedure, the hemodialysis procedure has been suggested as a potential source of inflammation in this patient population. Earof a hemodialysis procedure [9, 10]. This effect has been lier studies did not provide clear-cut evidence of the potential explained by the loss of amino acids and protein into the contribution of the hemodialysis procedure to inflammation, dialysate and by the blood-membrane interaction [11, 12]. as assessed by markers of inflammation such as cytokine levels Earlier studies have shown modest changes in selected and acute-phase protein production. cytokine concentrations before and after hemodialysis, Methods. Nine patients were studied using primed-constant infusion of l-(l-13 C) leucine 2 hours before, during, and 2 hours particularly with the use of bioincompatible membranes after a single hemodialysis session. We evaluated the effects [13-21]. Direct evidence of acute-phase response to the of hemodialysis on induction of interleukin-6 (IL-6) production hemodialysis procedure, especially with the use of bioas well as the fractional synthetic rates (FSR) of albumin and compatible hemodialysis membranes, is controversial. In fibrinogen, two well-known acute-phase proteins. Results. During hemodialysis, albumin FSR and fibrinogen order to explore this issue further, we evaluated the direct FSR increased significantly compared to the measurements effects of the hemodialysis procedure on the induction obtained during baseline period. During this period, albumin of inflammatory reaction by serial assessments of interand fibrinogen FSR increased 64% and 34%, respectively, comleukin-6 (IL-6) concentration and the fractional synthetic pared to baseline (P Ͻ 0.05). While the increase in IL-6 conrates (FSR) of two acute-phase reactants, namely serum centration was modest during hemodialysis (14%), the levels further increased at the end of the 2-hour post-hemodialysis albumin and serum fibrinogen before, during, and after period (68% higher compared to baseline, P Ͻ 0.05). Fibrinohemodialysis. IL-6 is considered to be a major regulator gen FSR also demonstrated a further increase during the postof many of the acute phase proteins including C-reactive dialysis period (17% higher compared to the intradialytic peprotein (CRP), albumin, and fibrinogen [22-24]. In addiriod and 58% higher compared to baseline), while albumin FSR tion, fibrinogen levels are often elevated in hemodialysis stabilized during this period. Conclusions. The results provide clear evidence of hemodi-patients and have been found to predict mortality [3, alysis-induced inflammatory response. The process is most no-25, 26]. Of note, fibrinogen FSR is increased in trauma table during the 2-hour post-hemodialysis period. patients who have high levels of inflammatory markers [27]. The results of our study indicate that the hemodialysis procedure induces an inflammatory response as evi-Chronic inflammation is highly prevalent in end-stage denced by the increase in fibrinogen FSR observed durrenal disease (ESRD) patients [1-3]. It is also strongly ing hemodialysis followed by concomitant increases in correlated with clinical outcome [3-5]. Chronic inflamboth IL-6 concentrations and fibrinogen FSR during the mation can be related to multiple factors in ESRD pa-2-hour post-hemodialysis period. tients, including underlying uremic conditions, reduced METHODS