Plasma tumor necrosis factor soluble receptors in chronic renal failure

Brockhaus, Manfred; Bar-Khayim, Y; Gurwicz, Swietlana; Frensdorff, Asher; Haran, Nurit

doi:10.1038/ki.1992.332

Cited by 98 publications

(65 citation statements)

References 46 publications

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“…The concentrations of both sTNFRs were calculated from the amount of bound labeled TNF using a I: I binding stoichiometry between TNF and sTNFR. The concentrations calculated in this way were consistent with those obtained by using recombinant sTNFRs as the standard [24]. The serum concentrations of TNF were determined by an assay (IRMA; Medgenix, Fleurus, Belgium).…”

Section: Methodssupporting

confidence: 57%

“…The specificity of the assays has been confirmed by experiments in which the binding of the detecting recombinant TNF to sTNFRs could be prevented either by addition of an excess (20~g/mL) of unlabeled TNF or by replacing the anti-TNFR monoclonal antibodies by nonspecific antibodies [24]. In addition, the linearity ofthe assays was verified using natural TNFRs from celllysates ofHL-60 cells and by recombinant TNFR-p55 and -p75.…”

Section: Methodsmentioning

confidence: 67%

“…In the circulation, however, from which TNF is cleared with a very short half-life [6], sTNFRs probably mainly act as inhibitors of excessive TNF activity, especially when they are present in relatively high concentrations [17,31]. Indeed, several in vitro studies have reported significant inhibition ofTNF activity by sTNFRs when present at a 10-to 100-fold molar excess, depending on the bioassay used [12,17,24,31]. In addition, administration of recombinant sTNFR-p55 to baboons with lethal bacteremia attenuates hemodynamic collapse and cytokine release [17].…”

Section: Discussionmentioning

confidence: 99%

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Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Poll

Jansen²,

Leenen³

et al. 1993

Journal of Infectious Diseases

115

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To assess the role of tumor necrosis factor (TNF) in the appearance of soluble TNF receptors (sTNFRs), 20 consecutive patients with a clinical diagnosis of sepsis were studied as were 7 chimpanzees after administration of endotoxin (4 ng/kg) with or without pentoxifylline. The patients had markedly elevated serum levels of sTNFR-p55 and sTNFR-p75 compared with healthy controls (P < .0001 for both receptors). The levels of both soluble receptors correlated with simultaneously measured immunoreactive TNF concentrations (p55: r = .63, P < .01; p75: r = .69, P < .001). In the chimpanzees, endotoxin induced subsequent rises in the serum concentrations ofTNF and sTNFRs. Although pentoxifylline reduced the TNF response to intravenous endotoxin to 20% (P < .05), the appearance of sTNFRs was only moderately inhibited (sTNFRp55 to 79% on average, P < .05; sTNFR-p75 to 77%, P = .12). These results indicate that TNF either does not play an important role in the appearance of sTNFRs in systemic infection or that a small amount of TNF remaining in the circulation after some bacterial challenges is sufficient to preserve the secretion of its soluble receptors.Sepsis is a syndrome characterized by hypotension, vascular leakage, and failure of multiple organs. Tumor necrosis factor (TNF) is an important factor for initiation ofthe septic syndrome [1 ]. Massive induction ofTNF synthesis, resulting in high concentrations of the protein in the circulation, is a prerequisite for the development of shock and multiple organ failure in experimental sepsis in animals [2]. In patients with sepsis, the extent of systemic TNF release correlates strongly with mortality rates [3,4]. Administration of TNF to animals or humans reproduces many of the features of septicemia [5,6]. Recently, naturally occurring inhibitors of TNF activity have been found in the urine of normal individuals and febrile patients and in the serum of patients with renal insufficiency [7][8][9][10][11]. These host mediators, originally termed TNF-binding proteins, have subsequently been identified as the soluble extracellular domains of the 55-and 75-kDa membrane-bound TNF receptors [12][13][14][15][16]. Soluble

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Section: Methodssupporting

confidence: 57%

Section: Methodsmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Poll

Jansen²,

Leenen³

et al. 1993

Journal of Infectious Diseases

115

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“…Various factors affect gastric motility in patients with CRF. Among these may be the increased levels of some GI hormones (Taylor et al, 1980;Wesdorp et al, 1981;Sirinek et al, 1984), several kinds of uremic toxin retention (Jones et al, 1969;Nakamura et al, 1990;DeDeyn et al, 1995;Anderstam et al, 1996), and a number of cytokines (Herbelin et al, 1991;Brockhaus et al, 1992;Kimmel et al, 1998;king et al, 1998) that appear in CRF patients. Some kinds of uremic toxin that can induce GI symptoms such as anorexia and bloating is excluded after the hemodialysis.…”

Section: Discussionmentioning

confidence: 99%

Improvement of gastric motility by hemodialysis in patients with chronic renal failure

Adachi

Kamiya

Hirako

et al. 2007

J. Smooth Muscle Res.

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Background: Gastrointestinal (GI) symptoms are common in patients with chronic renal failure (CRF). We have previously demonstrated that patients with predialysis endstage renal disease showed a high prevalence of GI symptoms and gastric hypomotility, and that gastric hypomotility appears to be an important factor in generating GI symptoms. However, it is not clear whether impaired gastric motor function would improve after hemodialytic treatment. Aims: To examine the relationship between gastric motor function and GI symptoms in CRF patients on hemodialysis. Methods: The study was performed in 19 patients with CRF treated with hemodialysis for more than six months and in 12 matched healthy controls. GI symptom severity was quantified in all patients. Gastric motility was evaluated with cutaneously recorded electrogastrography (EGG) and gastric emptying of semi-solid meals using the 13 C-acetic acid breath test. Results: Six patients had no symptoms, and 11 had slight GI symptoms with a total symptom score of less than 5. Compared with controls, CRF patients revealed no differences in gastric motility parameters, with the exception of a lower percentage of normogastria in EGG at fasting state. Eleven patients had normal gastric motor function (Group A), and eight showed abnormalities of either gastric myoelectrical activity or gastric emptying (Group B). There was no difference in symptom score between Group A and Group B. Conclusions: More than half of the patients with CRF on hemodialysis demonstrated normal gastric motility, and no or slight GI symptoms. Hemodialytic treatment may improve impaired gastric motility and reduce GI symptoms in patients with CRF.

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“…Some features of this cellular immunodeficiency are thought to result from a suppression of T helper cell type 1 (Th1) cytokines [9] and a defective costimulation of T cells via the B7-CD28 pathway [10]. Elevated circulating levels of cytokines and their corresponding receptors have been reported in the setting of chronic renal failure (CRF) [11][12][13][14][15][16][17], indicating that dysregulations in the cytokine network may be in part responsible for the development of uraemic immunodeficiency. In this study we investigated the in vivo presence of soluble CD40 and its possible changes in haemodialysis patients, CAPD patients and patients with CRF.…”

Section: Introductionmentioning

confidence: 99%

Soluble CD40 in the serum of healthy donors, patients with chronic renal failure, haemodialysis and chronic ambulatory peritoneal dialysis (CAPD) patients

Schwabe

Engelmann

Hess

et al. 1999

Clinical and Experimental Immunology

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SUMMARYCD40 and its ligand CD40L are key players in T cell-B cell interaction and T cell-antigen-presenting cell (APC) interaction. Inhibition of CD40-CD40L interaction leads to severe humoral and cellular immunodeficiency. In this study we examined the presence of soluble CD40 (sCD40) in the serum of haemodialysis (HD) patients, CAPD patients, chronic renal failure (CRF) patients and healthy donors in order to evaluate the possible involvement of CD40 in uraemic immunodeficiency. Soluble CD40 was detected in the serum of healthy donors (n ¼ 41) with a mean of 0·14 Ϯ 0·12 ng/ml and in the urine of healthy donors with a mean of 1·80 Ϯ 0·74 ng/ml. Soluble CD40 was highly elevated in all patients with impaired renal function. HD patients (n ¼ 22) had up to 100-fold elevated sCD40 levels with a mean concentration of 8·32 Ϯ 4·11 ng/ml, whereas CAPD patients (n ¼ 10) had considerably lower levels of sCD40 with a mean of 3·58 Ϯ 2·40 ng/ml. A strong correlation between sCD40 and serum creatinine levels was noted in CRF patients (n ¼ 66). The highly elevated levels of sCD40 may point to the involvement of CD40 and its ligand CD40L in the clinical manifestation of uraemic immunodeficiency.

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Plasma tumor necrosis factor soluble receptors in chronic renal failure

Cited by 98 publications

References 46 publications

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Release of Soluble Receptors for Tumor Necrosis Factor in Clinical Sepsis and Experimental Endotoxemia

Improvement of gastric motility by hemodialysis in patients with chronic renal failure

Soluble CD40 in the serum of healthy donors, patients with chronic renal failure, haemodialysis and chronic ambulatory peritoneal dialysis (CAPD) patients

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