scholarly journals Interleukin 6 (rs1800795) and pentraxin 3 (rs2305619) polymorphisms-association with inflammation and all-cause mortality in end-stage-renal disease patients on dialysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Susana Rocha ◽  
Maria João Valente ◽  
Susana Coimbra ◽  
Cristina Catarino ◽  
Petronila Rocha-Pereira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
End Stage Renal Disease ◽  
Inflammatory Biomarkers ◽  
Genotype Distribution ◽  
Pentraxin 3 ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Circulating Levels ◽  
Esrd Patients

AbstractChronic inflammation plays an important role in the progression and outcome of chronic kidney disease (CKD). The circulating levels of the inflammatory biomarkers interleukin 6 (IL6) and pentraxin 3 (PTX3) are enhanced in CKD patients, and are associated with the progression of the disease and with higher risk for cardiovascular events, the major cause of death in CKD patients. Our aim was to study how specific polymorphisms of IL6 and PTX3 encoding genes affect the inflammatory response and outcome of end-stage renal disease (ESRD) patients on dialysis. Methodology included the analysis of two single nucleotide polymorphisms (SNP), namely the IL6 (rs1800795) polymorphism in the promoter region (-174G > C), and the PTX3 (rs2305619) polymorphism in the intron 1 (+ 281A > G), which were analyzed in ESRD patients on dialysis and in a group of heathy individuals. The allelic frequencies, genotype distribution and their association with circulating levels of the inflammatory markers C-reactive protein (CRP), IL6, growth differentiation factor 15 (GDF15) and PTX3, were determined in ESRD patients. Events of death were recorded along one year, to assess the association of the studied SNPs with all-cause mortality and the inflammatory biomarkers, in ESRD patients. Results showed that the allelic frequencies and genotype distribution for IL6 and PTX3 SNPs in the control group and ESRD patients were similar and in agreement with other European reports. For the IL6 polymorphism, we found a trend towards higher levels of high-sensitivity (hs) CRP, IL6 and PTX3 in the homozygous genotypes; the CC genotype also showed the highest levels of GDF15. The mortality rate after the 1-year follow-up was 10.4%. The CC genotype (IL6 SNP) was associated to a higher risk of mortality and deceased patients carrying this genotype also showed the highest levels of hsCRP. Regarding the studied PTX3 SNP, the AA genotype was linked to an enhanced inflammatory response, showing the highest values of hsCRP and IL6. Nevertheless, this genotype had no significant impact on the mortality rate. In conclusion, both studied SNPs seem to modulate the inflammatory response in ESRD and may, therefore, be determinant on disease progression and patients’ outcome. Our data also highlights the importance of research on genetic variants that, although less frequent, may have significant biological value.

scholarly journals Interleukin 6 (rs1800795) and Pentraxin 3 (rs2305619) Polymorphisms - Association with Inflammation and All-Cause Mortality in End-stage-renal Disease Patients on Dialysis

2021 ◽  
Author(s):  
Susana Rocha ◽  
Maria João Valente ◽  
Susana Coimbra ◽  
Cristina Catarino ◽  
Petronila Rocha-Pereira ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Renal Disease ◽  
Interleukin 6 ◽  
End Stage Renal Disease ◽  
Pentraxin 3 ◽  
Allelic Frequencies ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Chronic inflammation plays an important role in the progression and outcome of chronic kidney disease (CKD). The inflammatory biomarkers interleukin-6 (IL6) and pentraxin 3 (PTX3) are enhanced in CKD patients and associated with progression of the disease and higher risk for cardiovascular events, the major cause of death in these patients. Our aim was to study how the polymorphisms of their encoding genes affect the inflammatory response and outcome of end-stage renal disease (ESRD) patients on dialysis. We analyzed two single nucleotide polymorphisms (SNP), the IL6 (rs1800795) polymorphism in the promoter region (-174G/C), and the PTX3 polymorphism in the intron 1 (+ 281A/G), in ESRD patients on dialysis and in heathy individuals. The allelic frequencies, genotype distribution and their association with the circulating levels of the inflammatory markers high sensitivity C-reactive protein (hsCRP), interleukin (IL6), growth differentiation factor 15 (GDF15) and PTX3, were determined in ESRD patients; events of death were recorded along one year to evaluate all-cause mortality and the association between inflammation and the studied polymorphisms. The allelic frequencies and genotyping distribution for IL6 and PTX3 in controls and ESRD patients were similar and in agreement with European reports. For the IL6 polymorphism, we found an association of the GG and CC genotype with higher IL6 levels; the CC genotype showed also high PTX3, hsCRP and GDF15 levels. For the PTX3 polymorphism, the AA genotype was linked to the highest values of hsCRP and IL6. The mortality rate after 1-year follow-up was 10.4%. The CC genotype (IL6 polymorphism), in deceased patients, was associated to increased levels of hsCRP, IL6 and PTX3, with low levels of GDF15 and with a highest mortality risk. The AA genotype for PTX3 polymorphism, in spite of the enhancement in inflammation, showed no significant impact on mortality. Our results show that the CC genotype of the IL6 polymorphism was associated with an enhanced inflammatory state and a poorer survival rate. Both IL6 and PTX3 polymorphisms seem to modulate the inflammatory response and, therefore, disease progression and outcome. Our data also highlights the importance of research on genetic variants that, although less frequent, may have significant biological value.

scholarly journals Long Pentraxin 3 as a Broader Biomarker for Multiple Risk Factors in End-Stage Renal Disease: Association with All-Cause Mortality

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Maria João Valente ◽  
Susana Rocha ◽  
Susana Coimbra ◽  
Cristina Catarino ◽  
Petronila Rocha-Pereira ◽  
...  
Keyword(s):  
End Stage Renal Disease ◽  
Renal Fibrosis ◽  
Pentraxin 3 ◽  
Dialysis Patients ◽  
Inflammatory Biomarker ◽  
Multiple Risk Factors ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Persistent inflammation in end-stage renal disease (ESRD) patients is known to underlie the progression of chronic kidney disease and to be associated with multiple risk factors including malnutrition, atherosclerosis, and cardiovascular disease (CVD). The acute-phase protein pentraxin 3 (PTX3) has a proven potential as a local inflammatory biomarker, but its clinical utility in ESRD remains unclear. Circulating levels of PTX3 and classical inflammatory mediators, including the clinical prototypical C-reactive protein (CRP), were assessed in 246 ESRD patients on dialysis and analysed in relation to the lipid profile, adipokine levels, and nutritional, cardiac, and renal fibrosis markers. Occurrence of deaths was recorded for the following year. Contrarily to the classical inflammatory markers, PTX3 levels were negatively correlated with nutritional markers and associated with a less atherogenic lipid profile. Levels of the cardiac and renal fibrosis markers and of the oxidized LDL/LDL-C ratio were found to be independent determinants of PTX3 concentration. When comparing inflammatory mediators, the increase in the PTX3 levels was the only predictor of all-cause mortality in dialysis patients in a survival model adjusted to all markers under study, other than the inflammatory ones, besides common confounding factors in dialysis. Data support the clinical applicability of PTX3 as a broader inflammatory biomarker than the classical ones, presenting a close association with inflammation, malnutrition, CVD, and renal fibrosis and a great potential to predict all-cause mortality in dialysis patients. The pleiotropic character of PTX3 may be of clinical relevance, and it could be targeted to ameliorate the high morbidity and mortality associated with ESRD.

Abstract 16854: End-Stage Renal Disease Associated With Metabolic Syndrome: A Study of Biomarkers Relevant to Cardiovascular Risk

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jawed Fareed ◽  
Vinod Bansal ◽  
Debra Hoppensteadt ◽  
Daneyal Syed ◽  
Syed Ahmad
Keyword(s):  
Metabolic Syndrome ◽  
End Stage Renal Disease ◽  
Inflammatory Process ◽  
C Peptide ◽  
Stage Renal Disease ◽  
End Stage ◽  
Metabolic Biomarkers ◽  
Circulating Levels ◽  
Esrd Patients ◽  
Pai 1

Introduction: Metabolic syndrome (MS) represents a cluster of cardiovascular risk factors which contribute to myocardial infarction and stroke in end stage renal disease (ESRD) patients. Several metabolic biomarkers have been identified and their circulating levels provide a better understanding of the pathogenesis of MS/ESRD. The purpose of this investigation is to profile biomarkers of MS in ESRD patients. Materials and Methods: Plasma samples from 87 patients with ESRD undergoing maintenance hemodialysis and 50 normals were collected prior to a routine session. These samples were profiled for metabolic biomarkers using protein chip bioarray technology. The protein chip array was comprised of several biomarkers of MS. All results were compiled in terms of group means +/- 1 SD (SEM) and statistically analyzed. Results: In comparison to the normal samples, the ESRD group showed marked increase in circulating levels of all biomarkers. TNFa (47.4 +/- 18.3 vs 4.1 +/- 1.1 ng/mL) and IL-6 (7.8 +/- 9.1 vs 0.8 +/- 0.4 ng/mL) showed the most pronounced increase. C-peptide (14.5 +/- 4.1 vs 2.8 +/- 1.6 ng/mL), leptin (29.7 +/- 29.2 vs 5.2 +/- 7.9 ng/mL), resistan (16.1 +/- 6.0 vs 2.3 +/- 0.7 ng/mL) and ferritin (274 +/- 57 vs 57 +/- 63 ng/mL) showed a 5-fold increase in the ESRD group compared to normal. PAI-1 (5.4 +/- 5.2 vs 2.9 +/- 2.5 ng/mL), IL-1a (1.3 +/- 1.7 vs 0.35 +/- 0.07 ng/mL) and insulin (32.1 +/- 17.3 vs 17.1 +/- 1.7 ng/mL) showed modest increase in the ESRD patients. The increase in all of the MS biomarkers in the ESRD patients were highly significantly elevated, p <0.05. Conclusion: The specific biochip array for MS allows the selective determination of various biomarkers associated with this syndrome in the ESRD patients and normals. Parallel increase in resistan, insulin, C-peptide, and leptin points to the derangement of glucose metabolism in these patients. Increase IL-1a, TNFa, and ferritin suggests the upregulation of an inflammatory process. PAI-1 increase suggests a fibrinolytic deficit. The parallel derangement of the inflammatory process and metabolic syndrome contributes to the cardiovascular and cerebrovascular complications in these patients.

P1239SHORT- AND LONG-TERM OUTCOME OF END-STAGE RENAL DISEASE PATIENTS WITH ACUTE MYOCARDIAL INFARCTION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Hirota Kida ◽  
Shungo Hikoso ◽  
Akihiro Sunaga ◽  
Oeun Bolrathanak ◽  
Takayuki Kojima ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
End Stage Renal Disease ◽  
Term Outcome ◽  
Long Term Outcome ◽  
All Cause Mortality ◽  
Short And Long Term ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Background and Aims End-stage renal disease (ESRD) patients frequently have the coronary artery disease. However, the short- and long-term outcome of ESRD patients with acute myocardial infarction (AMI) is little known. The aim of this study was to clarify it. Method Using the database of the Osaka Acute Coronary Insufficiency Study (OACIS), 8702 consecutive AMI patients (male: 75.2%, mean age: 66.9±12.2yrs) from 2002 to 2013 were analyzed. We classified these patients into two groups, those with ESRD [ESRD group (n=271)] and without ESRD [No-ESRD group (n=8431)] and examined in-hospital or long-term all-cause mortality. ESRD was defined as eGFR&lt;15ml/min/1.73m2. Results ESRD group had higher frequency of diabetes (59.3% vs 37.8%, p&lt;0.01), hypertension (90.1% vs 63.3%, p&lt;0.01), Killip class≧2 (40.1% vs 21%, p&lt;0.01), multi-vessel disease (69.3% vs 50.8%, p&lt;0.01), and lower frequency of peak CK&gt;3000 (21.7% vs 32.4%, p&lt;0.01) than No-ESRD group. Mean follow-up period was 1041±721 days. In hospital mortality of ESRD group was 27% and No-ESRD group 7.2%. In patients who discharged alive (8027 patients), 1-year mortality of ESRD group was 12.2% and No-ESRD group 3.3%, 3-year mortality of ESRD group was 29.3% and No-ESRD group 8.7%. Kaplan-Meier analysis revealed that the all-cause mortality (log-rank p&lt;0.01) was significantly higher in ESRD group than No-ESRD group. In ESRD patients who discharged alive (203patients), Cox univariate analysis after multiple imputation revealed that peak CK&gt;3000 was significantly associated with an increased risk of mortality (Hazard ratio 2.67, 95% confidence interval 1.18to 6.07, p=0.031). Conclusion In patients with AMI, ESRD was significantly associated with worse short- and long-term outcome, suggesting that careful treatment might be required in ESRD patients with AMI, especially had peak CK&gt;3000.

scholarly journals Cell-free DNA as a marker for the outcome of end-stage renal disease patients on haemodialysis

2020 ◽  
Author(s):  
Susana Coimbra ◽  
Susana Rocha ◽  
Henrique Nascimento ◽  
Maria João Valente ◽  
Cristina Catarino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
End Stage Renal Disease ◽  
Stress Markers ◽  
Free Dna ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients ◽  
And Oxidative Stress

Abstract Background DNA damage and inflammation are common in end-stage renal disease (ESRD). Our aim was to evaluate the levels of circulating cell-free DNA (cfDNA) and the relationship with inflammation, anaemia, oxidative stress and haemostatic disturbances in ESRD patients on dialysis. By performing a 1-year follow-up study, we also aimed to evaluate the predictive value of cfDNA for the outcome of ESRD patients. Methods A total of 289 ESRD patients on dialysis were enrolled in the study: we evaluated cfDNA, haemogram, serum iron, hepcidin, inflammatory and oxidative stress markers, and haemostasis. Events and causes of deaths were recorded throughout the follow-up period. Results ESRD patients, as compared with controls, presented significantly higher levels of cfDNA, hepcidin, and inflammatory and oxidative stress markers, and significantly lower values of iron and anaemia-related haemogram parameters. The all-cause mortality rate was 9.7%; compared with alive patients, deceased patients (n = 28) were older and presented significantly higher values of inflammatory markers and of cfDNA, which was almost 2-fold higher. Furthermore, cfDNA was the best predictor of all-cause mortality and cardiovascular mortality in ESRD patients, in both unadjusted and adjusted models for basic confounding factors in dialysis. Conclusions Our data show cfDNA to be a valuable predictive marker of prognosis in ESRD patients on dialysis treatment; high levels of cfDNA were associated with a poor outcome.

Longitudinal Causal Effects of Normalized Protein Catabolic Rate on All-Cause Mortality in Patients with End-Stage Renal Disease: Adjusting for Time-varying Confounders Using G-estimation Method

2020 ◽  
Author(s):  
Mohammad Aryaie ◽  
Hamid Sharifi ◽  
Azadeh Saber ◽  
Maryam Nazemipour ◽  
Mohammad Ali Mansournia
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Weibull Model ◽  
Time Varying ◽  
Catabolic Rate ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients ◽  
Protein Catabolic Rate

Abstract This study aimed to estimate causal effect of normalized protein catabolic rate (nPCR) on mortality among end stage renal disease (ESRD) patients in the presence of time-varying confounding affected by prior exposure using g-estimation. Information about 553 ESRD patients was retrospectively collected over 8 years, from 2011 to 2019, from hemodialysis facilities at Kerman, southeast of Iran. nPCR was dichotomized to &lt; 1.2 versus ≥ 1.2 g/kg per day. Then standard time-varying accelerated failure time (AFT) Weibull model was built, and results were compared with those generated by g-estimation. After appropriately adjusting for time-varying confounders, weighted g-estimation yielded 78% shorter survival time (95% confidence interval [95% CI]: -81% to -73%) in patients under continuous nPCR &lt; 1.2 than those who had nPCR ≥ 1.2 g/kg per day during the follow-up, though it was 18% (95% CI: -57% to +54%) in Weibull model. Moreover, the hazard ratio estimates of 4.56 (95% CI: 3.69 to 5.37), and 1.20 (95% CI: 0.66 to 2.17) were obtained by weighted g-estimation and Weibull model, respectively. G-estimation indicated that inadequate dietary protein intake characterized by nPCR increases all-cause mortality among ESRD patients, but the Weibull model provided a substantially biased effect estimate towards the null.

scholarly journals End-Stage Renal Disease and Critical Limb Ischemia: A Deadly Combination?

2012 ◽  
Vol 101 (2) ◽  
pp. 138-143 ◽  
Author(s):  
F. Biancari ◽  
E. Arvela ◽  
M. Korhonen ◽  
M. Söderström ◽  
K. Halmesmäki ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Disease ◽  
Lower Limb ◽  
End Stage Renal Disease ◽  
Bypass Surgery ◽  
Independent Predictor ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Objectives: This study was planned to evaluate the prognostic impact of end-stage renal disease (ESRD) in patients with critical leg ischemia (CLI) undergoing infrainguinal revascularization. Materials and Methods: 1425 patients who underwent infrainguinal revascularization for CLI were the subjects of the present analysis. Ninety-five patients had ESRD (eGFR < 15 ml/min/m2), and of them 66 (70%) underwent percutaneous transluminal angioplasty and 29 (30%) underwent bypass surgery. Results: ESRD patients had significantly lower overall survival (at 3-year, 27.1% vs. 59.7%, p < 0.0001), leg salvage (at 3-year, 57.7% vs. 83.0%, p<0.0001), and amputation free survival (at 3-year, 16.2% vs. 52.9%, p < 0.0001) than patients with no or less severe renal failure. The difference in survival was even greater between 86 one-to-one propensity matched pairs (at 3-year, 23.1% vs. 67.3%, p < 0.0001). ESRD was an independent predictor of all-cause mortality (RR 2.46, 95%CI 1.85–3.26). Logistic regression showed that age ≥ 75 years was the only independent predictor of 1-year all-cause mortality (OR 4.92, 95%CI 1.32–18.36). Classification and regression tree analysis showed that age ≥ 75 years and, among younger patients, bypass surgery for leg ulcer and gangrene were associated with significantly higher 1-year mortality. Conclusions: Lower limb revascularization in patients with CLI and end-stage renal failure is associated with favourable leg salvage. However, these patients have a very poor survival and this may jeopardize any attempt of revascularization. Further studies are needed to identify ESRD patients with acceptable life expectancy and who may benefit from lower limb revascularization.

scholarly journals MO810INTERLEUKIN-6 (-174G/C) POLYMORPHISM, RS1800795, IN ESRD PATIENTS' OUTCOME*

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Susana Rocha ◽  
Maria João Valente ◽  
Susana Coimbra ◽  
Cristina Catarino ◽  
Petronila Rocha-Pereira ◽  
...  
Keyword(s):  
Survival Time ◽  
Cox Regression ◽  
High Sensitivity ◽  
Genotype Distribution ◽  
Cox Regression Analysis ◽  
All Cause Mortality ◽  
Inflammatory State ◽  
Stage Renal Disease ◽  
Circulating Levels ◽  
Esrd Patients

Abstract Background and Aims Chronic inflammation plays an important role in the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). The single nucleotide polymorphism (SNP) in the promoter region (-174G/C) of interleukin-6 (IL6) gene regulates the levels of this cytokine, which have been associated with a poor outcome in several pathologies. Our aims were to determine, according to the genotype distribution of this polymorphism, the association between the inflammatory mediators, high sensitivity C-reactive protein (hsCRP), IL6, and pentraxin 3 (PTX3), shown to be increased in ESRD, and to estimate the risk for all-cause mortality over a period of one year. Method 289 ESRD patients on hemodialysis (high-flux hemodialysis and hemodiafiltration) were included in this study. Real-Time PCR TaqMan SNP genotyping assays were used to assess allelic frequencies of IL6 (rs1800795). We evaluated the circulating levels of PTX3, hsCRP and IL6 using commercially available kits. Deaths occurring along 1-year follow-up period were recorded, and the all-cause mortality hazard ratio (HR), according to IL6 polymorphisms in this patient cohort were determined by Cox regression analysis. A p &lt; 0.05 value was considered statistically significant. Results In all IL6 (-174G&gt;C) genotypes, hsCRP was positively and significantly correlated with IL6. For hsCRP and PTX3, a positive correlation with significance was only found for the GG genotype. All genotypes showed positive correlations between IL6 and PTX3 circulating levels, although only the GG genotype achieved a significant value. The Cox regression survival analysis for all-cause mortality in ESRD patients, using as reference the heterozygous patients for IL6 polymorphism, showed that CC patients presented a significant higher mortality risk, with a HR of 3.275 [1.165 to 9.204]. Moreover, the median survival time of CC patients (100 [54 - 138] days) was lower than that presented by the GG genotype patients (211 [83 - 290] days, p &lt; 0.05 vs. CC) and by the heterozygous patients (291 [72 - 332] days, p = 0.157 vs. CC). Conclusion We observed different correlation profiles between inflammatory biomarkers within each IL6 (-174G&gt;C) genotype. The association of the CC genotype of the IL6 polymorphism with a poorer outcome and shorter survival time for ESRD patients was also observed. However, further studies are required and must consider the underlying individual genetic background, since the inflammatory state appears to be influenced by IL6 polymorphisms, which, in turn, might be determinant for disease progression and outcome. Acknowledgments This work was supported by Applied Molecular Biosciences Unit-UCIBIO, financed by national funds from FCT/MCTES (UIDB/04378/2020), by North Portugal Regional Coordination and Development Commission (CCDR-N)/NORTE2020/Portugal 2020 (Norte-01-0145-FEDER-000024) and by REQUIMTE-Rede de Química e Tecnologia-Associação in the form of a researcher (S. Rocha) – project Dial4Life co-financed by FCT/MCTES (PTDC/MEC-CAR/31322/2017) and FEDER/COMPETE 2020 (POCI-01-0145-FEDER-031322).

A translational approach to micro-inflammation in end-stage renal disease: molecular effects of low levels of interleukin-6

2010 ◽  
Vol 119 (4) ◽  
pp. 163-174 ◽  
Author(s):  
Bruno Memoli ◽  
Simona Salerno ◽  
Alfredo Procino ◽  
Loredana Postiglione ◽  
Sabrina Morelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Renal Disease ◽  
Interleukin 6 ◽  
End Stage Renal Disease ◽  
Human Hepatocytes ◽  
Fetuin A ◽  
Stage Renal Disease ◽  
End Stage ◽  
Circulating Levels ◽  
Esrd Patients

Inflammation plays a key role in the progression of cardiovascular disease, the leading cause of mortality in ESRD (end-stage renal disease). Over recent years, inflammation has been greatly reduced with treatment, but mortality remains high. The aim of the present study was to assess whether low (<2 pg/ml) circulating levels of IL-6 (interleukin-6) are necessary and sufficient to activate the transcription factor STAT3 (signal transducer and activator of transcription 3) in human hepatocytes, and if this micro-inflammatory state was associated with changes in gene expression of some acute-phase proteins involved in cardiovascular mortality in ESRD. Human hepatocytes were treated for 24 h in the presence and absence of serum fractions from ESRD patients and healthy subjects with different concentrations of IL-6. The specific role of the cytokine was also evaluated by cell experiments with serum containing blocked IL-6. Furthermore, a comparison of the effects of IL-6 from patient serum and rIL-6 (recombinant IL-6) at increasing concentrations was performed. Confocal microscopy and Western blotting demonstrated that STAT3 activation was associated with IL-6 cell-membrane-bound receptor overexpression only in hepatocytes cultured with 1.8 pg/ml serum IL-6. A linear activation of STAT3 and IL-6 receptor expression was also observed after incubation with rIL-6. Treatment of hepatocytes with 1.8 pg/ml serum IL-6 was also associated with a 31.6-fold up-regulation of hepcidin gene expression and a 8.9-fold down-regulation of fetuin-A gene expression. In conclusion, these results demonstrated that low (<2 pg/ml) circulating levels of IL-6, as present in non-inflamed ESRD patients, are sufficient to activate some inflammatory pathways and can differentially regulate hepcidin and fetuin-A gene expression.

Abstract P391: Metabolic Syndrome Does Not Associate with an Increase Mortality in End Stage Renal Disease Patients: a Systematic Review and Meta-Analysis

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Sikarin Upala ◽  
Anawin Sanguankeo
Keyword(s):  
Metabolic Syndrome ◽  
Renal Function ◽  
End Stage Renal Disease ◽  
Meta Analysis ◽  
Residual Renal Function ◽  
All Cause Mortality ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients ◽  
Cvd Mortality

Background: Metabolic syndrome (Mets) is documented to increase mortality in the general population. However, there are reports of lower mortality in end stage renal disease (ESRD) patients with obesity. We conducted a meta-analysis to determine the association of all-cause and cardiovascular disease (CVD) mortality, and residual renal function with Mets in ESRD subjects. Objectives: PubMed/MEDLINE, EMBASE, and CENTRAL from their inception to September 2014 were comprehensively searched for eligible studies assessing the effects of the metabolic syndrome in ESRD subjects. Inclusion criterion was ESRD participants who had hemodialysis (HD or peritoneal dialysis (PD). Renal transplant subjects were excluded. Two authors independently assessed article quality and extracted the data. The primary outcome was all-cause mortality and secondary outcomes were CVD death and residual renal function. Results: From 23 full-text articles, 7 studies involving 613 (all-cause mortality), 284 (CVD death) and 383 (residual renal function) participants were included in the meta-analysis that was based on the random effects model. Compared with the non-Mets, ESRD subjects with Mets had no significant difference in risk of all-cause mortality (pooled odds ratio= 1.65; 95% CI, 0.86, 3.17) (figure 1) or CVD death (pooled odds ratio= 1.67; 95% CI, 0.75, 3.69). There was also no difference in residual renal function between the two groups with pooled standard mean difference of -0.26 ml/min/1.73 m2 (95% CI: -0.62, 0.10). Conclusion: Metabolic syndrome is not associated with an increased risk of all-cause or CVD mortality in ESRD patients who underwent HD or PD.

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