الفهرس 
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Abstract
Hemodialysis (HD) process is associated with increasing thrombotic trend especially due to platelets and clotting factors activation. Thrombotic episodes in HD patients are mainly related to a reduction in vascular access blood flow due to fibro muscular and intimal hyperplasia, which may result in vascular access stenosis.
The blood flow reduction causes blood stasis and favors hypercoagulability, hypotension and hypovolemia, predisposing to a prothrombotic environment.
ADAMTS13, a circulating metalloprotease, was first cloned and identified as a member of A Disintegrin And Metalloprotease with ThromboSpondin type 1 repeats (ADAMTS) family in 2001. It is primarily synthesized in hepatic stellate cells, but is also found in other cells including endothelial cells, and megakaryocytes or platelets.ADAMTS13 is secreted into plasma as a constitutively active enzyme at a plasma concentration of, approximately, 1 μg/ml. It cleaves a large adhesive glycoprotein, von Willebrand factor (VWF),that plays an essential role in primary hemostasis by recruiting platelets to the site of vessel injury.
It seems though, that ADAMTS13 and VWF levels imbalance is a common component of a hypercoagulability state in HD patients which, in addition to other genetic and acquired factors, could trigger the thrombotic events in these patients.
ADAMTS13 deficiency and/or the presence of antibodies against this enzyme may increase ULVWF plasma levels, favoring the occurrence of thrombosis in small vessels. Several studies have shown that diseases associated to low or absent activity of ADAMTS13, such
as thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS), compromise the VWF multimers cleavage, elevating the plasma levels of these factors and consequently the thrombotic risk.
Accordingly, the present study was designed to assess ADAMTS 13 plasma levels in patients under maintenance Hemodialysis (HD) to determine its role in the occurrence of vascular access thrombosis (VAT) in such patients.
This study was conducted on on 60 ESRD patients under regular hemodialysis for more than 6 months in Hemodialysis Units of Banha and Shebin Elkom teaching Hospitals –EGYPT, and 20 healthy individuals who served as a control.
Patients with malignancy, active infection, recent trauma or liver disease were excluded from the study.
All participants were thoroughly interrogated and examined clinically and were subjected to complete blood count, kidney function tests, liver function tests, lipid profile, FBS, PPBS, serum ADAMTS 13.
Dialysis patients (n = 60) were divided into 2 groups according to presence or absence of vascular access thrombosis. GI included 30 patients with vascular access thrombosis while GII included 30 patients without vascular access thrombosis.
Results of the study demonstrated that there is highly significant decrease in ADAMTS 13 levels in patients G I and GII compared to controls GIII.
ADAMTS 13 in studied patients according to type of vascular access showed a highly significant decrease in G I patients with VAT compared to GII patients.
Decreased ADAMTS 13 probably contributes to the hypercoagulability state seen in HD patients as detected in the study , a cut off level of ADAMTS 13 at 200 ng/ml is accurate (95.00%) for occurrence of VAT in group (I) patients with sensitivity of 96.67%%, specificity93.33%, PPV of93.55%and NPV of 96.55%.
Lipid profile in studied dialysis patients showed significant higher serum Cholesterol, Triglycerides and LDL in GI than GII patients.
Significant positive correlation was found between S.ADAMTS 13 and e-GFR in GI.
stepwise logistic regression analysis for VAT in studied patients conditioned on ADAMTS 13, potential risk factors and laboratory data was carried out to detect important predictors of VAT and results was presented as OR (0.92) and 95% CI (0.87 to 0.99) P=0.02.