Serum soluble Fas (CD95) and Fas ligand profiles in chronic kidney failure

Perianayagam, Mary C.; Murray, Susan; Balakrishnan, Vaidyanathapuram S.; Guo, Daoxia; King, Andrew J.; Pereira, Brian J.G.; Jaber, Bertrand L.

doi:10.1067/mlc.2000.109318

Cited by 39 publications

(39 citation statements)

References 27 publications

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“…In accordance with other studies we also found a dependency of sFas levels on kidney function [27] . In patients with chronic renal failure and in patients undergoing dialysis elevated sFas levels have been described.…”

Section: Discussionsupporting

confidence: 81%

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Elsing¹

2007

WJG

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AIM:To evaluate plasma levels of nitrite/nitrate (NOx), soluble Fas (sFas) antigen, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in patients with compensated and acute decompensated cirrhosis and to evaluate mediators causing acute decompensation in liver cirrhosis. METHODS:This prospective study was conducted in the medical intensive care unit of an academic tertiary center. Fifty-five patients with acute decompensation (gastrointestinal hemorrhage, encephalopathy, hydropic decompensation) and twenty-five patients with compensated liver cirrhosis were included. Blood samples were taken for analyses of sFas, Nox, IL-6, TNF-α. Liver enzymes and kidney functions were also tested. RESULTS:In patients with acute decompensation, plasma sFas levels were higher than in non-decompensated patients (15 305 ± 4646 vs 12 458 ± 4322 pg/mL, P < 0.05). This was also true for the subgroup of patients with alcoholic liver cirrhosis (P < 0.05). The other mediators were not different and none of the parameters predicted survival, except for ALT (alanine-aminotransferase). In patients with portal-hypertension-induced acute hemorrhage, NOx levels were significantly lower than in patients with other forms of decompensation (70.8 ± 48.3 vs 112.9 ± 74.9 pg/mL, P < 0.05). When NOx levels were normalized to creatinine levels, the difference disappeared. IL-6, TNF-α and sFas were not different between bleeders and non-bleeders. In decompensated patients sFas, IL-6 and NOx levels correlated positively with creatinine levels, while IL-6 levels were dependent on Child class. CONCLUSION:In acute decompensated cirrhotic patients sFas is increased, suggesting a role of apoptosis in this process and patients with acute bleeding have lower NOx levels. However, in this acute complex clinical situation, kidney function seems to have a predominant influence on mediator levels.

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Section: Discussionsupporting

confidence: 81%

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Elsing¹

2007

WJG

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“…In fact, it has been reported that Fas expression is increased at atherosclerotic plaque sites in humans [35]. It has also been shown that sFas binds the Fas ligand and inhibits apoptosis, and that the high levels of sFas in dialysis patients might be a compensatory response to minimize cell apoptosis [36]. In the present study, sFas was also correlated with Kt/V and residual renal function.…”

Section: Discussionsupporting

confidence: 62%

Coronary Artery Calcification, Systemic Inflammation Markers and Mineral Metabolism in a Peritoneal Dialysis Population

et al. 2006

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Aims: To assess the prevalence of coronary artery calcification (CAC) in peritoneal dialysis (PD) patients and to determine whether comorbidities such as inflammation, dyslipidemia and mineral metabolism disorders correlate with its development. Methods: Forty-nine PD patients (45% male; median age, 52 years) were submitted to multislice computed tomography. Inflammatory markers, anti-oxidized LDL antibody, calcium–phosphate balance and lipid profiles were assessed. Results: Twenty-nine patients (59.2%) presented CAC (median calcium score, 234.7 Agatston units). Patients with CAC were older than those without, more frequently presented a history of coronary artery disease or hypertension and had lower HDL cholesterol levels, as well as presenting higher levels of osteoprotegerin and LDL oxidation. The logistic regression revealed that the independent determinants of CAC were age (odds ratio = 1.12; p = 0.006) and number of prescribed anti-hypertensive drugs (odds ratio = 2.38; p = 0.048). When the population was stratified by calcium score quartile, soluble Fas levels were significantly higher in patients with severe calcification. In patients younger than 45, CAC correlated positively with phosphorus levels (r = 0.52; p = 0.04). Conclusion: In PD patients, CAC is highly prevalent. Our results indicate that conditions such as inflammation and mineral disturbances are associated with its development.

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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: 49%

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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Serum soluble Fas (CD95) and Fas ligand profiles in chronic kidney failure

Cited by 39 publications

References 27 publications

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Serum levels of soluble Fas, nitric oxide and cytokines in acute decompensated cirrhotic patients

Coronary Artery Calcification, Systemic Inflammation Markers and Mineral Metabolism in a Peritoneal Dialysis Population

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

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