Effect of the Hemodialysis Session on bcl-2 Expression in Peripheral Blood Mononuclear Cells in vivo

Koliousi, Elli; Vartholomatos, George; Katopodis, Konstantinos P.; Kolaitis, Nikolaos; Siamopoulos, Kostas C.

doi:10.1159/000097077

Cited by 4 publications

(5 citation statements)

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“…Existing data suggest that enhanced apoptosis appears in the progression of CKD and uremic milieu per se is partly responsible for the phenomenon [1,2,3,9,10]. We demonstrated that expression of Bcl-2 decreased significantly in the course of CKD which remained the only independent predictor.…”

Section: Discussionmentioning

confidence: 51%

“…Increased apoptosis of leukocytes has been described in hemodialysis (HD) and non-dialysis patients, while miscellaneous factors, such as, uremia, acidosis, oxidative stress, iron overload and malnutrition have been implicated [1,2,3]. In addition, a significant percentage of HD patients demonstrate an activated inflammatory response in the absence of any apparent cause [4,5].…”

Section: Introductionmentioning

confidence: 99%

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Mononuclear Leukocyte Apoptosis and Inflammatory Markers in Patients with Chronic Kidney Disease

et al. 2012

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Background/Aim: Increased apoptosis along with enhanced inflammation has been reported in hemodialysis and pre-dialysis patients. However, there is limited information at which stage during the progression of chronic kidney disease (CKD) the balance between pro- and anti-apoptotic mechanisms is disturbed and inflammatory response is activated. The aim of this study was to investigate possible alterations in apoptotic and inflammatory markers during CKD (stages 1–4) progression and the probable interactions between them. Methods: In a cross-sectional study, 152 steady-state CKD outpatients (83 males, 55%) with mean estimated glomerular filtration rate 46 (29–76) ml/min/1.73 m² were studied. Apoptosis was assessed in peripheral blood mononuclear cells by estimating Bcl-2 expression, annexin V-propidium iodine staining and serum soluble Fas (sFas) and Fas-ligand. Serum levels of C-reactive protein, tumor necrosis factor-α (TNF-α), interleukin-6 and plasma levels of fibrinogen were measured as markers of inflammation. Results: Bcl-2 expression was found to decrease significantly in both lymphocytes and monocytes from CKD stage 1 to 4. In contrast, the activity of sFas increased significantly and so did the levels of TNF-α and fibrinogen. The majority of these alterations occurred as soon as patients entered stage 3 of CKD. A multivariate regression analysis demonstrated that CKD remained a significant predictor of the aggregate of the assessed markers. Conclusions: Apoptosis appeared to increase across CKD stages 1–4, and this was associated with increased proinflammatory activity.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Mononuclear Leukocyte Apoptosis and Inflammatory Markers in Patients with Chronic Kidney Disease

et al. 2012

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“…Therefore, interpretation of pre-post studies has to be done carefully. This holds also true for a study that did not find differences in expression of the proto-oncogene bcl-2 in monocytes [108]. Since the expression increased in lymphocytes (thus indicating inflammatory activation) the lack of effect on monocytes might be caused by sequestration of the activated cells from the circulation.…”

Section: The Role Of Hemodialysis Treatment On Monocytes Phenotype and Functionmentioning

confidence: 79%

Monocytes in Uremia

Girndt

Trojanowicz

Ulrich

2020

Toxins

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Monocytes play an important role in both innate immunity and antigen presentation for specific cellular immune defense. In patients with chronic renal failure, as well as those treated with maintenance hemodialysis, these cells are largely dysregulated. There is a large body of literature on monocyte alterations in such patients. However, most of the publications report on small series, there is a vast spectrum of different methods and the heterogeneity of the data prevents any meta-analytic approach. Thus, a narrative review was performed to describe the current knowledge. Monocytes from patients with chronic renal failure differ from those of healthy individuals in the pattern of surface molecule expression, cytokine and mediator production, and function. If these findings can be summarized at all, they might be subsumed as showing chronic inflammation in resting cells together with limited activation upon immunologic challenge. The picture is complicated by the fact that monocytes fall into morphologically and functionally different populations and population shifts interact heavily with dysregulation of the individual cells. Severe complications of chronic renal failure such as impaired immune defense, inflammation, and atherosclerosis can be related to several aspects of monocyte dysfunction. Therefore, this review aims to provide an overview about the impairment and activation of monocytes by uremia and the resulting clinical consequences for renal failure patients.

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“…hand, the report in this issue of Blood Purification by Koliousi et al [5] evaluated the effect of a hemodialysis (HD) session using two different types of membrane (cellulosic and synthetic) on in vivo bcl-2 expression of lymphocytes and monocytes. bcl-2 expression increased significantly in lymphocytes after the HD procedure, irrespective of the membrane used.…”

Section: Is Bcl-2 a Key Molecule In The Abnormalmentioning

confidence: 99%

Is bcl-2 a Key Molecule in the Abnormal Immune Response of Hemodialysis Patients?

2006

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Effect of the Hemodialysis Session on bcl-2 Expression in Peripheral Blood Mononuclear Cells in vivo

Cited by 4 publications

References 36 publications

Mononuclear Leukocyte Apoptosis and Inflammatory Markers in Patients with Chronic Kidney Disease

Mononuclear Leukocyte Apoptosis and Inflammatory Markers in Patients with Chronic Kidney Disease

Monocytes in Uremia

Is bcl-2 a Key Molecule in the Abnormal Immune Response of Hemodialysis Patients?

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