Correlation between Oxidized Low Density Lipoproteins and von Willebrand Factor in Chronic Renal Failure

1996 ◽  
Vol 76 (05) ◽  
pp. 663-669 ◽  
Author(s):  
Paul Holvoet ◽  
Jan Donck ◽  
Michèle Landeloos ◽  
Els Brouwers ◽  
Kristel Luijtens ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Wide Spectrum ◽  
Endothelial Injury ◽  
Maintenance Hemodialysis ◽  
Apo B ◽  
The Individual ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryAn ELISA specific for a wide spectrum of oxidized apo B-100 in OxLDL was developed and applied to blood samples from 27 control subjects, 20 mild chronic renal failure (MCRF) patients, 21 severe chronic renal failure patients on conservative treatment (SCRF) and 56 severe chronic renal failure patients on maintenance hemodialysis (HEMO). Mean levels of OxLDL were 0.59 mg/dl in controls (95% Cl, 0.52-0.66 mg/dl), and were 2.7-fold (p <0.01), 3.1-fold (p <0.001) and 5.4-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Levels of von Willebrand factor, a marker of endothelial injury, were 100 percent in controls (95% Cl, 90-110 percent), and were 1.5-fold (p = NS), 1.6-fold (p <0.01) and 2.1-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Multiple regression analysis revealed that the extent of renal failure (F = 14; p = 0.0004) accounted for a significant fraction of the variation in OxLDL levels, also after exclusion of patients with evidence of ischemic atherosclerotic disease (F = 21; p = 0.0001). After adjustment for the extent of renal failure, hemodialysis (F = 5.6; p = 0.021) and LDL cholesterol levels (F = 7.1, p = 0.0095) contributed significantly to the variation in OxLDL levels. Whereas the extent of renal failure contributed only marginally to the individual variations in vWF levels (F = 4.1; p = 0.048), these levels correlated significantly with plasma levels of OxLDL (F=26; p=0.0001). In conclusion, atherogenic OxLDL increase progressively during the development of renal failure suggesting that the oxidation of LDL may be associated with endothelial injury and atherogenesis in these patients.

A Study of Bleeding Time and Von Willebrand Factor in Patients with Chronic Renal Failure

1990 ◽  
Vol 79 (s23) ◽  
pp. 11P-11P
Author(s):  
GTM Robinson ◽  
LR Bond ◽  
S Talbot ◽  
A Chietole ◽  
DH Sevan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Bleeding Time ◽  
Von Willebrand ◽  
Willebrand Factor

Arteriovenous Fistula Obstruction and Expression of Platelet Receptors for Von Willebrand Factor and for Fibrinogen (Glycoproteins GPIb and GPIIb/llla) in Hemodialysis Patients

1996 ◽  
Vol 19 (8) ◽  
pp. 451-454 ◽  
Author(s):  
M. Liani ◽  
F. Salvati ◽  
E. Tresca ◽  
G. Dl Paolo ◽  
L. Vitacolonna ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Von Willebrand Factor ◽  
Hemodialysis Patients ◽  
Platelet Surface ◽  
Surface Receptors ◽  
Platelet Receptors ◽  
Stage Renal Disease ◽  
Von Willebrand ◽  
Willebrand Factor

Platelet surface receptors for von Willebrand factor and for fibrinogen (glycoproteins GPIb and GPIIb/llla) were studied with monoclonal antibodies CD42 and CD41 and cytofluorometry in 31 healthy subjects, 10 hemodialysis patients with no A-V fistula obstruction (patent original fistula), 10 hemodialysis patients with frequent A-V fistula obstruction (more than twice), 12 patients with mild chronic renal failure (creatinine 1.75±0.40 mg/100ml), 11 patients with advanced chronic renal failure (creatinine 5.62±1.22 mg/100ml), and 10 patients with end-stage renal disease (ESRD) treated with peritoneal dialysis. There was a significant increase of platelet surface glycoproteins GPIb and GPIIb/llla in the population of hemodialysis patients with frequent A-V fistula obstruction. The expression of these platelet receptors might be related to the prothrombotic tendency of a group of patients with ESRD, who suffer more occlusive and thrombotic events of the A-V fistula. This group of patients may also have a higher frequency of systemic thrombotic and atherosclerotic complications.

scholarly journals The functions of the A1A2A3 domains in von Willebrand factor include multimerin 1 binding

2016 ◽  
Vol 116 (07) ◽  
pp. 87-95 ◽  
Author(s):  
D'Andra Parker ◽  
Subia Tasneem ◽  
Richard Farndale ◽  
Dominique Bihan ◽  
J. Sadler ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Von Willebrand Factor ◽  
Platelet Adhesion ◽  
Structural Features ◽  
High Shear ◽  
The Individual ◽  
Static Conditions ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryMultimerin 1 (MMRN1) is a massive, homopolymeric protein that is stored in platelets and endothelial cells for activation-induced release. In vitro, MMRN1 binds to the outer surfaces of activated platelets and endothelial cells, the extracellular matrix (including collagen) and von Willebrand factor (VWF) to support platelet adhesive functions. VWF associates with MMRN1 at high shear, not static conditions, suggesting that shear exposes cryptic sites within VWF that support MMRN1 binding. Modified ELISA and surface plasmon resonance were used to study the structural features of VWF that support MMRN1 binding, and determine the affinities for VWF-MMRN1 binding. High shear microfluidic platelet adhesion assays determined the functional consequences for VWF-MMRN1 binding. VWF binding to MMRN1 was enhanced by shear exposure and ristocetin, and required VWF A1A2A3 region, specifically the A1 and A3 domains. VWF A1A2A3 bound to MMRN1 with a physiologically relevant binding affinity (KD: 2.0 ± 0.4 nM), whereas the individual VWF A1 (KD: 39.3 ± 7.7 nM) and A3 domains (KD: 229 ± 114 nM) bound to MMRN1 with lower affinities. VWF A1A2A3 was also sufficient to support the adhesion of resting platelets to MMRN1 at high shear, by a mechanism dependent on VWF-GPIbD binding. Our study provides new information on the molecular basis of MMRN1 binding to VWF, and its role in supporting platelet adhesion at high shear. We propose that at sites of vessel injury, MMRN1 that is released following activation of platelets and endothelial cells, binds to VWF A1A2A3 region to support platelet adhesion at arterial shear rates.

scholarly journals Cerebral Endothelial Injury in Elderly Patients With Severe Head Injury Measured by Serum Thrombomodulin and von Willebrand Factor

2007 ◽  
Vol 47 (9) ◽  
pp. 383-388 ◽  
Author(s):  
Hiroyuki YOKOTA ◽  
Takahiro ATSUMI ◽  
Takashi ARAKI ◽  
Akira FUSE ◽  
Hidetaka SATO ◽  
...  
Keyword(s):  
Head Injury ◽  
Elderly Patients ◽  
Von Willebrand Factor ◽  
Severe Head Injury ◽  
Endothelial Injury ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Demonstration of Rickettsia conorii-induced endothelial injury in vivo by measuring circulating endothelial cells, thrombomodulin, and von Willebrand factor in patients with Mediterranean spotted fever [see comments]

Blood ◽  
1993 ◽  
Vol 82 (7) ◽  
pp. 2109-2116
Author(s):  
F George ◽  
P Brouqui ◽  
MC Boffa ◽  
M Mutin ◽  
M Drancourt ◽  
...  
Keyword(s):  
Von Willebrand Factor ◽  
Spotted Fever ◽  
Clinical Manifestations ◽  
Endothelial Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Rickettsia Conorii ◽  
Mediterranean Spotted Fever ◽  
Von Willebrand ◽  
Willebrand Factor

The endothelial cell (EC) is the primary target for Rickettsia conorii (RC) in Mediterranean spotted fever (MSF). Clinical manifestations such as thrombosis and vasculitis are mediated by pathologic changes localized in blood vessels. To study the in vivo endothelial injury induced by RC, markers of endothelial damage, including circulating EC (CEC), plasmatic thrombomodulin (TM), and von Willebrand factor (vWF), were investigated in 12 patients with MSF. CEC were counted in whole blood by a new immunomagnetic separation assay using a specific anti-EC antibody, S-Endo 1. Plasmatic TM and vWF antigens were measured by enzyme-linked immunosorbent assay. High levels of CEC and cell fragments were found in patients with a severe or malignant form of MSF. Sequential studies of CEC showed a decrease from 162 +/- 454 cells/mL before treatment to 6 +/- 7 cells/mL during treatment and recovery. Mean plasma TM and vWF levels that were also elevated before therapy (TM, 106 +/- 27 ng/mL; vWF, 420% +/- 164%) decreased progressively (TM, 55 +/- 43 ng/mL; vWF, 148% +/- 26%) during treatment. The measurement of cellular and molecular markers of vascular damage such as CEC, plasmatic TM, and vWF contributes to the definition of the Rickettsia-induced endothelial injury in vivo.

scholarly journals Monocytes in Uremia

Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 340 ◽  
Author(s):  
Matthias Girndt ◽  
Bogusz Trojanowicz ◽  
Christof Ulrich
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Current Knowledge ◽  
Large Body ◽  
Immune Defense ◽  
Maintenance Hemodialysis ◽  
Resting Cells ◽  
Small Series ◽  
Clinical Consequences ◽  
The Individual

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.

Contributions of Asn2198, Met2199, and Phe2200 in the factor VIII C2 domain to cofactor activity, phospholipid-binding, and von Willebrand factor-binding

2003 ◽  
Vol 89 (05) ◽  
pp. 795-802 ◽  
Author(s):  
Deborah Lewis ◽  
Mary Pound ◽  
Thomas Ortel
Keyword(s):  
Factor Viii ◽  
Von Willebrand Factor ◽  
Hydrophobic Surface ◽  
C2 Domain ◽  
Mutant Proteins ◽  
Phospholipid Binding ◽  
Cofactor Activity ◽  
The Individual ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe crystal structure of the factor VIII C2 domain consists of a β-sandwich core from which β-hairpins and loops extend to form a hydrophobic surface. The hydrophobic surface includes M2199 and F2200 at the tip of the 1st β-hairpin. To determine the individual contributions of residues N2198, M2199, and F2200 to phospholipid and von Willebrand factor (vWF) binding properties of factor VIII, we prepared mutant proteins with single alanine substitutions. We found that single mutations at N2198 and M2199 had relatively little impact on cofactor activity, or phospholipid and vWF binding. However the F2200A mutant had slightly lower cofactor activity at subsaturating phospholipid concentrations. Competitive ELISAs suggested that F2200 plays a more important role in both phospholipid-binding and vWF-binding than N2198 and M2199. All mutant proteins were still recognized by a monoclonal antibody and two factor VIII inhibitors that neutralized cofactor activity and blocked factor VIII binding to phospholipids.Presented in part at the XVIII Congress of the International Society on Thrombosis and Haemostasis, Paris, France, 6-12 July 2001, and the 43rd Annual Meeting of the American Society of Hematology, Orlando, Florida, 7-11 December 2001

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