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      Current tools for prediction of arteriovenous fistula outcomes

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          Abstract

          It remains challenging to accurately predict whether an individual arteriovenous fistula (AVF) will mature and be useable for haemodialysis vascular access. Current best practice involves the use of routine clinical assessment and ultrasonography complemented by selective venography and magnetic resonance imaging. The purpose of this literature review is to describe current practices in relation to pre-operative assessment prior to AVF formation and highlight potential areas for future research to improve the clinical prediction of AVF outcomes.

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          Clinical practice guidelines for vascular access.

          (2006)
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            Patency rates of the arteriovenous fistula for hemodialysis: a systematic review and meta-analysis.

            Angham Al Mutair, Sarah D Kosa, J. Zhang … (2014)
            Advantages of the arteriovenous fistula (AVF), including long patency and few complications, were ascertained more than 2 decades ago and may not apply to the contemporary dialysis population. Systematic review and meta-analysis. Estimates were pooled using a random-effects model and sources of heterogeneity were explored using metaregression. Patients treated with long-term hemodialysis using an AVF. English-language studies indexed in MEDLINE between 2000 and 2012 using prospectively collected data on 100 or more AVFs. Age, AVF location, and study location. Outcomes of interest were primary AVF failure and primary and secondary patency at 1 and 2 years. 7,011 citations were screened and 46 articles met eligibility criteria (62 unique cohorts; n = 12,383). The rate of primary failure was 23% (95% CI, 18%-28%; 37 cohorts; 7,393 AVFs). When primary failures were included, the primary patency rate was 60% (95% CI, 56%-64%; 13 studies; 21 cohorts; 4,111 AVFs) at 1 year and 51% (95% CI, 44%-58%; 7 studies; 12 cohorts; 2,694 AVFs) at 2 years. The secondary patency rate was 71% (95% CI, 64%-78%; 10 studies; 11 cohorts; 3,558 AVFs) at 1 year and 64% (95% CI, 56%-73%; 6 studies; 11 cohorts; 1,939 AVFs) at 2 years. In metaregression, there was a significant decrease in primary patency rate in studies that started recruitment in more recent years. Low quality of studies, variable clinical settings, and variable definitions of primary AVF failure. In recent years, AVFs had a high rate of primary failure and low to moderate primary and secondary patency rates. Consideration of these outcomes is required when choosing a patient's preferred access type. Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
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              A Self-Fulfilling Prophecy: C-Reactive Protein Attenuates Nitric Oxide Production and Inhibits Angiogenesis

              Subodh Verma, Chao-Hung Wang, Shu-Hong Li … (2002)
              Background— Given the central importance of nitric oxide (NO) in the development and clinical course of cardiovascular diseases, we sought to determine whether the powerful predictive value of C-reactive protein (CRP) might be explained through an effect on NO production. Methods and Results— Endothelial cells (ECs) were incubated with recombinant CRP (0 to 100 μg/mL, 24 hours), and NO and cyclic guanosine monophosphate (cGMP) production was assessed. The effects of CRP on endothelial NO synthase (eNOS) protein, mRNA expression, and mRNA stability were also examined. In a separate study, the effects of CRP (25 μg/mL) on EC cell survival, apoptosis, and in vitro angiogenesis were evaluated. Incubation of ECs with CRP resulted in a significant inhibition of basal and stimulated NO release, with concomitant reductions in cGMP production. CRP caused a marked downregulation of eNOS mRNA and protein expression. Actinomycin D studies suggested that eNOS downregulation was related to decreased mRNA stability. In conjunction with a decrease in NO production, CRP inhibited both basal and vascular endothelial growth factor–stimulated angiogenesis as assessed by EC migration and capillary-like tube formation. CRP did not induce EC survival but did, however, promote apoptosis in a NO-dependent fashion. Conclusions— CRP, at concentrations known to predict adverse vascular events, directly quenches the production of the NO, in part, through posttranscriptional effect on eNOS mRNA stability. Diminished NO bioactivity, in turn, inhibits angiogenesis, an important compensatory mechanism in chronic ischemia. Through decreasing NO synthesis, CRP may facilitate the development of diverse cardiovascular diseases. Risk reduction strategies designed to lower plasma CRP may be effective by improving NO bioavailability.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Kidney J
                Journal ID (iso-abbrev): Clin Kidney J
                Journal ID (publisher-id): ckj
                Journal ID (hwp): ndtplus
                Title: Clinical Kidney Journal
                Publisher: Oxford University Press
                ISSN (Print): 2048-8505
                ISSN (Electronic): 2048-8513
                Publication date (Print): June 2015
                Publication date (Electronic): 02 April 2015
                Publication date PMC-release: 02 April 2015
                Volume: 8
                Issue: 3
                Pages: 282-289
                Affiliations
                [1 ]Department of Vascular Access and Renal Transplantation, University Hospitals Birmingham, Queen Elizabeth Hospital , Birmingham B15 2TH, UK
                [2 ]Regional Nephrology Unit, Belfast Health and Social Care Trust, Belfast City Hospital , Belfast BT9 7AB, UK
                [3 ]School of Medicine, Dentistry and Biomedical Sciences, Health Sciences Building , Belfast BT9 7BL, UK
                Author notes
                Correspondence to: Damian G. McGrogan; E-mail: damianmcg@ 123456gmail.com ; damian.mcgrogan@ 123456uhb.nhs.uk
                Article
                Publisher ID: sfv019
                DOI: 10.1093/ckj/sfv019
                PMC ID: 4440466
                PubMed ID: 26034589
                SO-VID: cd3fdb9e-6365-4035-8c4e-a6ca199e8026
                Copyright © © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 2 January 2015
                Date accepted : 5 March 2015
                Categories
                Subject: Contents
                Subject: Vascular Access

                ScienceOpen disciplines: Nephrology
                Keywords: arteriovenous fistula,clinical assessment,definitions,ultrasonography,venography
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: arteriovenous fistula, clinical assessment, definitions, ultrasonography, venography

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