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      Assessment of Haemostatic Risk Factors in Patients with Acute Renal Failure Associated with Severe Systemic Inflammatory Response Syndrome

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          Abstract

          Background/Aim: The prognosis of acute renal failure (ARF) in the Intensive Care Unit (ICU) is variable and depends mainly on the underlying disease. Consequently, the outcome prediction is difficult. The majority of the prognostic measures used include clinical parameters and routine laboratory tests but not no study has considered the prognostic value of haemostatic disturbances. These disturbances play a key role in the evolution of multiple organ dysfunction syndrome (MODS) in patients with ARF, which occurs as part of systemic inflammatory response syndrome (SIRS). The aim of the present study was to search for early significant predictive factors among a group of haemostatic parameters in these patients. Methods: Forty patients (age: 60.1 ± 14.1 years) with ARF (requiring renal replacement therapy) associated with SIRS and haemodynamic instability (systolic blood pressure <90 mm Hg and/or vasopressor drugs) were included. The plasmatic levels of the following haemostatic factors were measured within the first 6 h of the SIRS evolution: von Willebrand Factor (vWF), thrombomodulin, plasminogen activity inhibitor type 1 (PAI-1 antigen), tissue type plasminogen activator (t-PA antigen), prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complexes (TAT) and D-dimer. Age, sex, medical or surgical disease, septic status or not, type of ARF (prerenal or acute tubular necrosis, oliguric or nonoliguric), and requirement for inotropics and mechanical ventilation were also considered. Univariate and multivariate logistic regressions were used to identify the risk factors for death and to develop a possible mortality prediction model on this basis. Results: By univariate analysis, high levels of PAI-1 antigen (≧60 ng/ml) and F1 + 2 (>2.5 nmol/l) at early phases of ARF-severe SIRS were found to be independent risk factors for death (odds ratio (OR) = 6.37, p = 0.0181 and OR = 5.49, p = 0.0238, respectively). Age over 61 years and requirement of mechanical ventilation were independent death risk factors (OR = 4.33, p = 0.0251 and OR = 2.4, p = 0.0078, respectively). A possible mortality prediction model was obtained including the age and the PAI-1 antigen and F1 + 2 variables. Conclusion: In patients with ARF associated with severe SIRS, the independent risk factors from the early phases of the process are not only the known variables such as advanced age, but also high levels of PAI-1 antigen and F1 + 2. In the future, the individual probability of death could be calculated by a prediction model which includes these variables.

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          Most cited references 3

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          Prognostic stratification in critically ill patients with acute renal failure requiring dialysis.

          Despite the widespread availability of dialytic and intensive care unit technology, the probability of early mortality in critically ill persons with acute renal failure is distressingly high. Previous efforts to predict outcome in this population have been limited by small sample size and the absence of uniform exclusion criteria. Additionally, data obtained decades ago may not apply today owing to changes in case mix. The medical records of 132 consecutive patients in the intensive care unit with acute renal failure who required dialysis from 1991 through 1993 were evaluated by a blinded reviewer. The overall in-hospital mortality rate was 70%. Twelve readily available historical, clinical, and laboratory variables were significantly associated with in-hospital mortality. Multivariate logistic regression analysis showed that mechanical ventilation, malignancy, and nonrespiratory organ system failure were independently associated with in-hospital mortality. Using a 95% positivity criterion, this model identified 24% of high-risk patients who died, without misclassification of any survivors. Of those who survived to hospital discharge, 33% were dialysis dependent and 28% were institutionalized long-term. Among critically ill patients, acute renal failure requiring dialysis is an ominous condition with a high risk of in-hospital mortality. This risk appears to depend largely on comorbid conditions, such as the need for mechanical ventilation and underlying malignancy. While this prognostic model requires prospective validation, it appears to identify a substantial fraction of patients for whom dialysis may be of limited or no benefit.
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            Elimination of interleukin 6 attenuates coagulation activation in experimental endotoxemia in chimpanzees

             al et,  H. S. Cate,  M Levi (1994)
            The role of interleukin 6 (IL-6) in the toxic sequelae of sepsis is controversial. To assess the part of IL-6 in inflammatory responses to endotoxin, we investigated eight chimpanzees after either a bolus intravenous injection of Escherichia coli endotoxin (n = 4; 4 ng/kg) or after the same dose of endotoxin with a simultaneous bolus intravenous injection of an anti-IL-6 mAb (30 mg; n = 4). Anti-IL-6 did not affect the induction of the cytokine network (tumor necrosis factor [TNF], soluble TNF receptors types I and II, and IL-8) by endotoxin, nor did it influence the occurrence of a neutrophilic leukocytosis and neutrophil degranulation, as monitored by the measurement of elastase- alpha 1-antitrypsin complexes. In contrast, anti-IL-6 markedly attenuated endotoxin-induced activation of coagulation, monitored with the plasma levels of the prothrombin fragment F1+2 and thrombin- antithrombin III complexes, whereas activation of fibrinolysis, determined with the plasma concentrations of plasmin-alpha 2- antiplasmin complexes, remained unaltered. We conclude that IL-6 does not have a feedback effect on the release of other cytokines after injection of endotoxin, and that it is not involved in endotoxin- induced neutrophilia or neutrophil degranulation. IL-6 is, however, an important intermediate factor in activation of coagulation in low grade endotoxemia in chimpanzees.
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              Acute renal failure in intensive care units--Causes, outcome, and prognostic factors of hospital mortality

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                Author and article information

                Journal
                NEF
                Nephron
                10.1159/issn.1660-8151
                Nephron
                S. Karger AG
                1660-8151
                2235-3186
                2002
                September 2002
                14 August 2002
                : 92
                : 1
                : 97-104
                Affiliations
                aDepartment of Nephrology, bDepartment of Hematology, and cThrombosis and Haemostasis Research Unit, University Clinic of Navarra, School of Medicine, University of Navarra, Pamplona, Spain
                Article
                64472 Nephron 2002;92:97–104
                10.1159/000064472
                12187091
                © 2002 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: 1, Tables: 3, References: 45, Pages: 8
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/64472
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