Lupus-Like in vitro Anticoagulant Activity in End-Stage Renal Disease

Nephron ◽  
1988 ◽  
Vol 49 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Carlos Quereda ◽  
Ana Pardo ◽  
Santiago Lamas ◽  
Luis Orofino ◽  
Angel Carcía-Avello ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Anticoagulant Activity ◽  
Stage Renal Disease ◽  
End Stage

Differences between KT/V Measured during Dialysis and KT/V Predicted from Manufacturer Clearance Data

1992 ◽  
Vol 15 (8) ◽  
pp. 465-469 ◽  
Author(s):  
L.K. Saha ◽  
J.C. Van Stone
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Urea Clearance ◽  
Blood Flows ◽  
The Mean ◽  
Stage Renal Disease ◽  
End Stage

We retrospectively analyzed data from 3,863 dialysis treatments in 329 end-stage renal disease patients over a period of 33 months to evaluate the accuracy of in vitro KT/V estimated by manufacturer's urea clearance data in relation to in vivo measured KT/V. In 1,087 urea clearances measured, mean actual clearance was 87% of predicted. At all blood flows, actual clearances were significantly lower than predicted (8-16% lower than predicted). In 2,807 KT/V measurements, predicted KT/V was 1.238 ± 0.005 whereas the mean of actual measured KT/V was 16% lower or 1.024 ± 0.005 (P < 0.0001). At different blood flows and with different dialyzers, predicted KT/V overestimated actual values. With increasing numbers of reuse, actual/predicted clearance ratios and actual/predicted KT/V ratios progressively dropped. Prescribing dialysis treatments using manufacturer's in vitro generated clearance data can lead to marked underdialysis of patients.

Endothelial Microparticles and Their Binding to Leukocytes in Patients with End-Stage Renal Disease.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3939-3939
Author(s):  
David Zuckerman ◽  
Mark Hofmeyer ◽  
Julio A. Chirinos ◽  
Wenche Jy ◽  
Joaquin J. Jimenez ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Neutrophil Activation ◽  
In Vitro Studies ◽  
Cd11b Expression ◽  
Endothelial Microparticles ◽  
Stage Renal Disease ◽  
End Stage ◽  
Normal Controls

Abstract Background: End-stage renal disease (ESRD) has been associated with endothelial dysfunction, a proinflammatory state and markedly increased cardiovascular risk. Endothelial microparticles (EMP) are released by activated or apoptotic endothelial cells. In vitro studies have shown that EMP can bind and activate neutrophils, suggesting that they may represent not only markers of endothelial status but also mediators of inflammation. The objectives of this study were to: Assess the levels of free EMP and leukocyte-bound EMP in ESRD; Determine whether EMP binding to neutrophils predicts the degree of neutrophil activation in patients with ESRD. Methods: We measured the levels of endothelial microparticles (EMP) and EMP-leukocyte conjugates in 80 patients with ESRD and 35 normal controls. We performed flow cytometry in peripheral venous blood before hemodialysis to measure (1) EMP positive for CD31 (EMP31), E-selectin (EMP62E), CD54 (EMP54); (2) EMP54- and EMP62E-leukocyte conjugates; (3) Neutrophil activation, assessed by expression of activation marker CD11b. Results: Assessment of free EMP revealed that patients with ESRD had slightly elevated levels of free EMP54 but not of free EMP62E or EMP31. However, levels of EMP54-Lymphocyte, EMP54-Monocyte, EMP54-Neutrophil, EMP62E-Lymphocyte and EMP62E-Monocyte conjugates were clearly elevated in patients with ESRD. CD11b expression in leukocytes strongly correlated with levels of EMP54-Neutrophil conjugates (R=0.67; p&lt;0.0001) and EMP62E-Neutrophil conjugates (R=0.66; p&lt;0.0001). Furthermore, both types of conjugates independently predicted CD11b expression (adjusted p&lt;0.05). Conclusions: ESRD is associated with increased binding of EMP to leukocytes, resulting in normal levels of some species of free EMP. Therefore, measurement of both free EMP and EMP-leukocyte conjugates is necessary for adequately assessing EMP release in ESRD. Levels of EMP bound to neutrophils strongly predict neutrophil activation, suggesting that EMP induce neutrophil activation in vivo, consistent with in vitro studies. EMP may represent important mediators of the proinflammatory state in ESRD. EMP and EMP-Leukocyte Conjugates in ESRD patients compared to normal controls ESRD (n=80) Controls (n=35) P value IQR=Interquartile range EMP31 (IQR) 842 (484–1546) 807 (566–1240) 0.97 EMP62E (IQR) 69 (39–128) 60 (43–113) 0.96 EMP54 (IQR) 75 (33–144) 34 (18–141) 0.04 EMP54-Lymphocyte Conjugates (±SD) 1.45±0.2 1.21±0.1 &lt;0.0001 EMP54-Monocyte Conjugates (±SD) 1.77±0.6 1.27±0.3 &lt;0.0001 EMP54-Neutrophil Conjugates (±SD) 2.12±0.6 1.85±0.6 0.02 EMP62E-Lymphocyte Conjugates (±SD) 1.30±0.2 1.13±0.1 &lt;0.0001 EMP62E-Monocyte Conjugates (±SD) 1.61±0.5 1.40±0.3 0.01 EMP62E-Neutrophil Conjugates (±SD) 2.04±0.6 2.05±0.5 0.95

Increased Levels of Anaphylatoxin (C5a) and Bradykinin in End-Stage Renal Disease Patients on Maintenance Hemodialysis. Potential Relevance to Heparin Mediated Hemodynamic Responses

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4079-4079
Author(s):  
Cafer Adiguzel ◽  
Vinod Bansal ◽  
Josephine Cunanan ◽  
Evangelos Litinas ◽  
Debra Hoppensteadt ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Sandwich Elisa ◽  
Maintenance Hemodialysis ◽  
Control Group ◽  
Contact Activation ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Besides the upregulation of inflammatory mediators, end stage renal disease (ESRD) patients maintained on hemodialysis are subjected to periodic exposure to heparin and contact activation due to procedural settings. Recently the presence of a heparin contaminant, namely hypersulfated chondroitin sulfate was linked with the adverse reactions and deaths observed in these patients (Kishmoto, et al. N J Med 2008). To validate this report we measured both the C5a anaphlatoxin and bradykinin levels in ESRD patients prior to and after maintenance hemodialysis. The control group comprised of 40 normal healthy individuals were included to establish the normal level of these mediators. A sandwich ELISA method utilizing a monoclonal antibody which is specific for human C5a and bradykinin were used in these studies. Both the C5a and bradykinin were elevated in pre-dialysis samples from ESRD patients (C5a: 3.2±0.6 ng/ml vs 14.2± 4.6 ng/ml, bradykinin: 6.4±1.8 ng/ml vs 9.3±2.4 ng/ml). Moreover, dialysis itself produced an increase in both the C5a and bradykinin levels. Moreover, the postdialysis samples were further increased, suggesting that dialysis and heparinization itself result in the up-regulation of these mediators. Supplementation of heparin to the plasma also resulted in the generation of both C5a and bradykinin. The plasma samples included in these studies represents patients who were not treateded with the contaminant heparin. Additional studies on in-vitro generation of these markers with contaminated heparin and the isolated contaminant showed that both of these triggered the generation of C5a and bradyknin. These results suggest that both C5a and bradykinin are up-regulated in ESRD patients and this level can be further augmented by dialysis and heparinization. Therefore, additional factors may have contributed to the complex adverse reaction profiles and deaths in patients administrated with contaminated heparin.

Vimentin cleavage in end-stage renal disease is not related to apoptosis

Open Medicine ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. 297-301 ◽  
Author(s):  
Felix Liebscher ◽  
Tobias Arnold ◽  
Ying Liang ◽  
Thomas Reiter ◽  
Georg Böhmig ◽  
...  
Keyword(s):  
Renal Disease ◽  
Healthy Volunteers ◽  
End Stage Renal Disease ◽  
Caspase 3 ◽  
Vimentin Expression ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

AbstractAnti-vimentin auto-antibodies contribute to chronic allograft nephropathy. They exist in sera of end-stage renal disease patients on hemodialysis (ESRD) already before renal transplantation. We found recently that a 49 kDa vimentin fragment is increased in lymphocytes of ESRD patients which is presented on the cell surface. In vitro studies showed that such a fragment is formed during apoptosis by active caspase-3. We hypothesized that vimentin degradation in leukocytes of ESRD patients correlates to caspase-3 activation in vivo. Lymphocytes and monocytes were isolated from ESRD patients and from healthy volunteers and analyzed for vimentin expression and caspase-3 activation. In addition, apoptosis was induced in vitro and quantified by flow cytometry. ESRD monocytes have shown only the full length 60 kDa vimentin isoform. ESRD lymphocytes, however, showed in addition a strongly increased expression of the 49 kDa vimentin in all samples. Caspase-3 activation was found in 60% of ESRD lymphocytes and 66% of ESRD monocytes but not in healthy volunteers. UV-mediated induction of apoptosis was not associated with vimentin degradation. These experiments could confirm increased vimentin degradation in ESRD lymphocytes. However, we could not validate any correlation to apoptosis.

scholarly journals Increased carbamylation level of HDL in end-stage renal disease: carbamylated-HDL attenuated endothelial cell function

2016 ◽  
Vol 310 (6) ◽  
pp. F511-F517 ◽  
Author(s):  
Jia Teng Sun ◽  
Ke Yang ◽  
Lin Lu ◽  
Zheng Bin Zhu ◽  
Jin Zhou Zhu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Paraoxonase 1 ◽  
Healthy Control ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

It is thought that carbamylated modification plays a crucial role in the development and progression of cardiovascular disease (CVD) in patients with end-stage renal disease (ESRD). However, information on the biological effects of carbamylated high-density lipoprotein (C-HDL) in ESRD is poor. The present study investigated the carbamylation level of HDL in ESRD and the effects of C-HDL on endothelial repair properties. HDL was isolated from healthy control subjects ( n = 22) and patients with ESRD ( n = 30). The carbamylation level of HDL was detected using ELISA. Isolated C-HDL for use in tissue culture experiments was carbamylated in vitro to a similar extent to that observed in ESRD. Human arterial endothelial cells were treated with C-HDL or native HDL to assess their migration, proliferation, and angiogenesis properties. HDL-associated paraoxonase 1 activity was also determined by spectrophotometry assay. Compared with healthy control subjects, the carbamylation level of HDL in ESRD patients was increased and positively correlated with blood urea concentration. In vitro, C-HDL significantly inhibited migration, angiogenesis, and proliferation in endothelial cells. Mechanistic studies revealed that HDL-associated paraoxonase 1 activity was decreased and negatively correlated with the carbamylation level of HDL in ESRD patients. In addition, C-HDL suppressed the expression of VEGF receptor 2 and scavenger receptor class B type I signaling pathways in endothelial cells. In conclusion, the present study identified a significantly increased carbamylation level of HDL in ESRD. Furthermore, C-HDL inhibited endothelial cell repair functions.

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