IL-1beta, TNF-alpha and IL-6 release from monocytes in haemodialysis patients in relation to dialytic age

Malaponte, Grazia; Bevelacqua, Valentina; Fatuzzo, Pasquale; Rapisarda, Francesco; Emmanuele, Giovanni; Travali, Salvatore; Mazzarino, María Clorinda

doi:10.1093/ndt/17.11.1964

Cited by 61 publications

(48 citation statements)

References 17 publications

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“…In addition, TNF-α levels were not very high even in the patients with other signs of inflammation, as also reported by others (33,34). It is interesting to note that CRP levels after the change of the water purification system correlated closely with the previous CRP levels, suggesting that the patients present a pattern of inflammatory activity dependent on other factors.…”

Section: Discussionsupporting

confidence: 82%

Dialysis water treated by reverse osmosis decreases the levels of C-reactive protein in uremic patients

Thomé

Senger

Garcez

et al. 2005

Braz J Med Biol Res

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Atherosclerosis is a major complication of chronic renal failure. Microinflammation is involved in atherogenesis and is associated with uremia and dialysis. The role of dialysate water contamination in inducing inflammation has been debated. Our aim was to study inflammatory markers in patients on chronic dialysis, before and 3 to 6 months after switching the water purification system from deionization to reverse osmosis. Patients had demographic, clinical and nutritional information collected and blood drawn for determination of albumin, ferritin, C-reactive protein (CRP), interleukin-6, and tumor necrosis factor-α in both situations. Acceptable levels of water purity were less than 200 colony-forming units of bacteria and less than 1 ng/ml of endotoxin. Sixteen patients died. They had higher median CRP (26.6 vs 11.2 mg/dl, P = 0.007) and lower median albumin levels (3.1 vs 3.9 g/l, P < 0.05) compared to the 31 survivors. Eight patients were excluded because of obvious inflammatory conditions. From the 23 remaining patients (mean age ± SD: 51.3 ± 13.9 years), 18 had a decrease in CRP after the water treatment system was changed. Overall, median CRP was lower with reverse osmosis than with deionization (13.2 vs 4.5 mg/l, P = 0.022, N = 23). There was no difference in albumin, cytokines, subjective global evaluation, or clinical and biochemical parameters. In conclusion, uremic patients presented a clinically significant reduction in CRP levels when dialysate water purification system switched from deionization to reverse osmosis. It is possible that better water treatments induce less inflammation and eventually less atherosclerosis in hemodialysis patients.

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Section: Discussionsupporting

confidence: 82%

Dialysis water treated by reverse osmosis decreases the levels of C-reactive protein in uremic patients

Thomé

Senger

Garcez

et al. 2005

Braz J Med Biol Res

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“…344 Activated macrophages exacerbate the inflammatory process by producing additional cytokines such as tumor necrosis factor 1α and interleukin 6. 345 Furthermore, they destroy renal tissue by phagocytosis and promote fibrosis by producing pro-fibrotic cytokines, such as transforming growth factor β1. [346][347][348] The net result of prolonged hypoxia is that a vicious pathological cycle is initiated in which fibroblast and inflammatory cell activation combine with apoptosis, endothelial proliferation, and epithelial-mesenchymal transition to cause tubulointerstitial fibrosis.…”

Section: The Hypoxia Death Cyclementioning

confidence: 99%

“…261,262 A second dogma in the field of leukocyte function was that hypoxia induces their adhesion not as a consequence of their sensing oxygen deprivation directly but only indirectly as a consequence of sensing inflammatory cytokines released by hypoxic tissue. [344][345][346] Again, this dogma was challenged by demonstrating that during hypoxia leukocytes exhibit an intrinsic increase in β2-integrin gene expression. 261,262 Following activation by hypoxia, recent evidence indicates that leukocytes exacerbate the inflammatory microenvironment.…”

Section: A New Hypoxia Paradigmmentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

125

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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“…It has been suggested that some dialysis-related alteration in the immune and host-defense system may be relevant, as they seem to correlate to the high production of proinflammatory cytokines (8). Moreover, the type of dialysis membrane has been suggested to play a role (9) as well as time on dialysis, as it correlated negatively with cytokine release (10). Next, the hemodialysis (HD) procedure itself may be involved.…”

mentioning

confidence: 99%

Effect of an Increase in C-Reactive Protein Level during a Hemodialysis Session on Mortality

Korevaar¹,

Manen

Dekker

et al. 2004

Journal of the American Society of Nephrology

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Abstract. The prevalence of chronic inflammation is high in dialysis patients. Moreover, it is associated with an increased mortality risk, yet the origin of chronic inflammation in dialysis patients remains unclear. The aim of this study was to determine the effect of a hemodialysis session (HD) on C-reactive protein (CRP) levels and to study the relation with survival. As part of a large, prospective, multicenter study in the Netherlands (Netherlands Cooperative Study on the Adequacy of Dialysis), patients who were started on dialysis treatment between September 1997 and May 1999 were included. Demographic data, clinical data, and serum samples were collected at regularly timed intervals. From this cohort, a random sample of patients was taken. CRP levels were determined before and after an HD session and before the next session. Date of death or censoring was recorded until September 2002. A total of 186 HD patients were included. Mean age was 65 yr (SD, 13); 56% were male. A total of 71 patients had a CRP level below the detection limit (3 mg/L), 68 patients showed no increase in CRP during an HD session (no-increase group), and 47 (25%) patients showed an increase in CRP level during an HD session (increase-group). No statistically difference in mean CRP levels before the dialysis session was found between the increase group (22.3 mg/L) and the no-increase group (19.4 mg/L). In the subsequent interdialytic period, CRP levels returned to the levels of the initial CRP value. Two-year survival was 44% in the increase group and 66% in the noincrease group (P ϭ 0.09). Independent of CRP level before the session and adjusted for age, comorbidity, nutritional status, and primary kidney disease, a raise of 1 mg/L CRP during a session was associated with a 9% increased mortality risk (adjusted hazard ratio, 1.09; 95% CI, 1.02 to 1.16). The present study showed an increase in CRP level during a single dialysis session in 25% of the patients; during the succeeding interdialytic period, CRP level returned to its original value. More important, however, an increase in CRP level during an HD session was independently associated with a higher mortality risk.

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IL-1beta, TNF-alpha and IL-6 release from monocytes in haemodialysis patients in relation to dialytic age

Abstract: These results indicate that prolonged treatment with dialysis can be considered a form of chronic stress that causes the progressive activation of monocytes, which ultimately leads to monocyte exhaustion and dysfunction.

Cited by 61 publications

References 17 publications

Dialysis water treated by reverse osmosis decreases the levels of C-reactive protein in uremic patients

Dialysis water treated by reverse osmosis decreases the levels of C-reactive protein in uremic patients

Hypoxia: The Force that Drives Chronic Kidney Disease

Effect of an Increase in C-Reactive Protein Level during a Hemodialysis Session on Mortality

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