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      Tissue Factor, Its Pathway Inhibitor, and Metabolic Disturbances in Long-Term Peritoneal Dialysis

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          Abstract

          Background/Aim: The tissue factor (TF) plays a key role in triggering the coagulation system in vivo. Our study was designed to determine whether or not the plasma levels of TF and its pathway inhibitor (TF pathway inhibitor; TFPI) in patients with chronic renal failure (CRF) treated by peritoneal dialysis (PD) (1) are pathologically altered; (2) differ between diabetics and nondiabetics, and (3) depend on the metabolic disorders associated with CRF and/or diabetes. Methods: Using ELISA, plasma TF and TFPI levels were measured once in 21 PD patients (10 with diabetes, 11 without diabetes) and in 21 healthy subjects. Results: As compared with healthy subjects (TF 282 pg/ml; TFPI 73 ng/ml), both TF and TFPI levels were significantly higher in PD patients with diabetes (485 pg/ml, p < 0.001, and 106 ng/ml, p < 0.01, respectively) and in PD patients without diabetes (480 pg/ml, p < 0,001, and 121 ng/ml, p < 0.001, respectively). The difference between diabetics and nondiabetics was not significant. In stepwise regression analysis, the TF levels depended on serum creatinine (partial correlation 0.39, p < 0.05), glycemia (0.43, p < 0.01), and insulin (–0.43, p < 0.05), and the TFPI levels depended on creatinine (partial correlation 0.67, p < 0.001), apolipoprotein B (0.46, p < 0.01), and plasma fibrinogen (0.43, p < 0.01). Conclusions: CRF patients on PD show increased plasma TF and TFPI levels. There is no difference between diabetics and nondiabetics. The TF and TFPI levels depend significantly on the renal function, as assessed by serum creatinine, and on some metabolic disorders. Elevated TF and TFPI levels may be related to thrombosis and atherosclerosis in CRF patients on PD.

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          Most cited references 9

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          Subendothelial retention of atherogenic lipoproteins in early atherosclerosis.

          Complications of atherosclerosis are the most common cause of death in Western societies. Among the many risk factors identified by epidemiological studies, only elevated levels of lipoproteins containing apolipoprotein (apo) B can drive the development of atherosclerosis in humans and experimental animals even in the absence of other risk factors. However, the mechanisms that lead to atherosclerosis are still poorly understood. We tested the hypothesis that the subendothelial retention of atherogenic apoB-containing lipoproteins is the initiating event in atherogenesis. The extracellular matrix of the subendothelium, particularly proteoglycans, is thought to play a major role in the retention of atherogenic lipoproteins. The interaction between atherogenic lipoproteins and proteoglycans involves an ionic interaction between basic amino acids in apoB100 and negatively charged sulphate groups on the proteoglycans. Here we present direct experimental evidence that the atherogenicity of apoB-containing low-density lipoproteins (LDL) is linked to their affinity for artery wall proteoglycans. Mice expressing proteoglycan-binding-defective LDL developed significantly less atherosclerosis than mice expressing wild-type control LDL. We conclude that subendothelial retention of apoB100-containing lipoprotein is an early step in atherogenesis.
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            Tissue-factor antigen and activity in human coronary atherosclerotic plaques.

            Coronary atherosclerotic-plaque thrombosis is a key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque rupture or fissuring frequently occurs in atherosclerosis, only a small proportion of ruptured plaques develop thromboses. Tissue-factor antigen and activity were measured in atherectomy samples from 50 consecutive patients with coronary artery disease (stable angina n = 19, unstable angina n = 24, and myocardial infarction n = 7). Median tissue-factor antigen and activity concentrations were significantly higher in plaques from patients with unstable angina and myocardial infarction than in those from patients with stable angina (antigen: 66.1 pg/mg [interquartile range 43.8-82.5] vs 32.4 pg/mg [9.8-43.4], p = 0.0001; activity: 0.22 mU/mg [0.17-0.41] vs 0.13 mU/mg [0.05-0.16], p = 0.0004). Tissue-factor, an initiator of the coagulation cascade, may account for the different thrombotic responses to the rupture of human coronary atherosclerotic plaques.
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              Tissue factor pathway inhibitor and the revised theory of coagulation.

               G Broze (1994)
              Tissue factor pathway inhibitor (TFPI) is a multivalent, Kunitz-type plasma proteinase inhibitor that regulates tissue factor-induced coagulation. TFPI directly inhibits activated factor X and, in a factor Xa-dependent fashion, produces feedback inhibition of the factor VIIa/tissue factor catalytic complex. The properties of this rediscovered inhibitor appear, at least in part, to explain the clinical requirement for both the extrinsic and intrinsic pathways of the cascade and waterfall theories of blood clotting and have led to a reformulation of the coagulation mechanism. In the revised hypothesis, factor VIIa/tissue factor is responsible for the initiation of coagulation, but owing to TFPI-mediated inhibition, sustained hemostasis requires the persistent and amplified procoagulant action of intrinsic factors VIII, IX, and XI.
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                Author and article information

                Journal
                KBR
                Kidney Blood Press Res
                10.1159/issn.1420-4096
                Kidney and Blood Pressure Research
                S. Karger AG
                1420-4096
                1423-0143
                2003
                2003
                19 November 2003
                : 26
                : 5-6
                : 368-375
                Affiliations
                Departments of aInternal Medicine I and bClinical Biochemistry and Laboratory Diagnostics, Charles University Medical School, Pilsen, Czech Republic
                Article
                73944 Kidney Blood Press Res 2003;26:368–375
                10.1159/000073944
                14610342
                © 2003 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 2, Tables: 5, References: 36, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/73944
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