HEMODIALYSIS DOWN REGULATES THE INFLAMMATORY MEDIATORS IN PATIENTS WITH END STAGE RENAL DISEASE

2007 ◽  
Vol 5 ◽  
pp. P-S-468-P-S-468
Author(s):  
V. Bansal ◽  
D. Hoppensteadt ◽  
J. Cunanan ◽  
R.S. Bajwa ◽  
C. Patel ◽  
...  
Keyword(s):  
Renal Disease ◽  
Inflammatory Mediators ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals SP306UP-REGULATION OF INFLAMMATORY MEDIATORS AND MARKERS OF METABOLIC DERAIGNMENT IN END STAGE RENAL DISEASE AS STUDIED BY BIOCHIP ARRAY ANALYSIS

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii480-iii480
Author(s):  
Vinod Bansal ◽  
Daneyal Syed ◽  
Debra Hoppensteadt ◽  
Mushabar Syed ◽  
Jawed Fareed
Keyword(s):  
Renal Disease ◽  
Inflammatory Mediators ◽  
End Stage Renal Disease ◽  
Array Analysis ◽  
Stage Renal Disease ◽  
End Stage

Upregulation of Inflammatory Mediators In End-Stage Renal Disease as Measured Via Biochip Array Technology

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 5186-5186
Author(s):  
Vinod Bansal ◽  
Rachael Davis ◽  
Evangelos Litinas ◽  
Debra Hoppensteadt ◽  
Indermohan Thethi ◽  
...  
Keyword(s):  
Renal Disease ◽  
Inflammatory Mediators ◽  
End Stage Renal Disease ◽  
Conflicts Of Interest ◽  
Fold Increase ◽  
Endothelial Damage ◽  
Cellular Damage ◽  
Array Technology ◽  
Stage Renal Disease ◽  
End Stage

Abstract Abstract 5186 End-Stage Renal Disease (ESRD) is a complex syndrome in which systemic vascular pathophysiologic changes contribute to adverse cardiovascular and cerebrovascular manifestations. Cardiovascular disease alone is present in over 60% of patients with ESRD and contributes heavily to mortality among this population. Given that inflammatory and hemostatic aberrations contribute to the overall pathogenesis of the syndrome, the purpose of this study is to profile several inflammatory mediators in order to better understand their role in the underlying mechanism of vascular changes in ESRD. Plasma samples from 49 patients with ESRD were collected prior to maintenance hemodialysis sessions. A group of 56 normal individuals, both male and female, was included as control. Cerebral Array II chips were used in the Randox® system to simultaneously measure Neuron Specific Enolase (NSE), Neutrophil Gelatinase-associated Lipocalin (NGAL), Soluble Tumor Necrosis Factor Receptor I (TNFRI), D-Dimer (DD), Thrombomodulin (TM), and C-reactive protein (CRP). The Randox® Evidence Investigator™ is a new biochip array technology that utilizes multiple discrete test regions of immobilized antibody to simultaneously quantify multiple markers from a single patient plasma sample based on the light signal generated from each test region. The data was statistically analyzed using the Mann-Whitney U test (two-tailed with Gaussian approximation). As compared to the normal individual, all of the markers studied showed an upregulation in patients with ESRD. Most notably, TNFRI showed a 19.8 fold increase in patients with ESRD (mean 7.8 ± 2.8 ng/ml, range 0.8 to 13.7) compared to the control (mean 0.4 ± 0.2, range 0.1 to 1.0). TM was increased 5.2 fold (mean 6.5 ± 2.6, range 0.7 to 14.1) compared to control (mean 1.2 ± 0.4, range 0.6 to 2.3). Also, NGAL showed a 4.6 fold increase (mean 1390 ± 257, range 406 to 1729), compared to control (mean 299 ± 99, range 115 to 603), and CRP a 4.2 fold increase (mean 5.7 ± 4.2 ug/ml, range 0.6 to 13.2) compared to control (mean 1.4 ± 1.7, range 0.2 to 11.4). DD and NSE were also increased 3.0 and 1.8 fold respectively. These studies show that some newer markers such as TNFRI, NGAL and NSE are upregulated in ESRD. The marked increase in TM is highly suggestive of endothelial damage. Similarly, the increase in TNFRI supports a state of increased cellular damage. The elevations in NGAL and CRP imply a state of increased inflammation and indicate a polypathologic process, which may predispose ESRD patients to both cardiovascular and cerebrovascular thromboembolic events. Finally, this study further validates the role of endothelial damage and endogenous thrombotic processes in ESRD as evidenced by the increased levels of TM and DD. However, the clinical significance of these markers still needs to be further explored. Disclosures: No relevant conflicts of interest to declare.

Acute effect of one session of hemodiafiltration with endogenous reinfusion on uremic toxins and inflammatory mediators

2020 ◽  
Vol 43 (7) ◽  
pp. 437-443
Author(s):  
Xiaohong Chen ◽  
Bo Shen ◽  
Xuesen Cao ◽  
Fangfang Xiang ◽  
Jianzhou Zou ◽  
...  
Keyword(s):  
Renal Disease ◽  
Inflammatory Mediators ◽  
End Stage Renal Disease ◽  
Uremic Toxins ◽  
Nutrient Loss ◽  
Infusion Therapy ◽  
Acute Effects ◽  
Long Term Treatment ◽  
Stage Renal Disease ◽  
End Stage

Aims: To investigate the acute effects of hemodiafiltration with endogenous infusion on the elimination of uremic toxins and inflammatory mediators in patients with end-stage renal disease. Materials and methods: A total of 37 end-stage renal disease patients undergoing chronic hemodialysis received a single hemodiafiltration with endogenous infusion dialysis treatment. The acute effects of one hemodiafiltration with endogenous infusion session on uremic toxins and inflammatory mediators were assessed by comparing the pre- and post-hemodiafiltration with endogenous infusion concentrations. Results: Hemoglobin and albumin were stable during hemodiafiltration with endogenous infusion therapy. The mean reduction ratios of β2-microglobulin, p-cresyl sulfate, and indoxyl sulfate were 43.60%, 40.91%, and 43.64%, respectively. Tumor necrosis factor-α also decreased significantly at a mean rate of 28.10%, while the concentrations of interleukin-6 and high-sensitivity C-reactive protein remained unchanged after one session of hemodiafiltration with endogenous infusion. Conclusion: The hemodiafiltration with endogenous infusion system is a new dialysis technique that combines diffusion, convection, and adsorption processes. It allows for extensive solute removal, including protein-bound uremic toxins and some pro-inflammatory cytokines, but does not cause nutrient loss and inflammatory response during the treatment. Although the effect after a single hemodiafiltration with endogenous infusion session is limited, it may be improved by repeated and long-term treatment.

Preeclampsia Tied to Later End-Stage Renal Disease

Ob Gyn News ◽  
2007 ◽  
Vol 42 (24) ◽  
pp. 7
Author(s):  
ROBERT FINN
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage

Parathyroid Dysfunction in End Stage Renal Disease

1980 ◽  
Vol 13 (1) ◽  
pp. 193-201
Author(s):  
Philip J. DìTella ◽  
Gordon R. Lang
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Parathyroid Dysfunction ◽  
Stage Renal Disease ◽  
End Stage

441 Neurohumoral activity, heart failure and prognosis in patients with end stage renal disease treated by chronic haemodialysis

2006 ◽  
Vol 5 (1) ◽  
pp. 105-105
Author(s):  
J SPINAR ◽  
O LUDKA ◽  
J VITOVEC ◽  
L SPINAROVA ◽  
D SOBOTOVA ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Chronic Haemodialysis ◽  
Stage Renal Disease ◽  
End Stage

Pathophysiology and Treatment of Hyperhomocysteinemia in End-Stage Renal Disease Patients

2001 ◽  
Vol 5 (1) ◽  
pp. 86-91
Author(s):  
G. Sunder-Plassmann ◽  
Walter H. Hörl
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Stage Renal Disease ◽  
End Stage
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