Evidence map›Paper›PMID 25309636›Full record

ArticleThe open urology & nephrology journal2014

Hemodynamic Shear Stress and Endothelial Dysfunction in Hemodialysis Access.

Michelle K Fitts, Daniel B Pike, Kasey Anderson, Yan-Ting Shiu

Open access · diamondAbstract read
In one paragraph

Article in The open urology & nephrology journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
8.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 67 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Michelle K FittsDepartment of Bioengineering, University of Utah, Salt Lake City, Utah, USA.
Daniel B PikeDepartment of Bioengineering, University of Utah, Salt Lake City, Utah, USA.
Kasey AndersonDepartment of Bioengineering, University of Utah, Salt Lake City, Utah, USA.
Yan-Ting ShiuDepartment of Medicine, Division of Nephrology and Hypertension, University of Utah, Salt Lake City, Utah, USA.
University of Utah · US

Funding

PREVENTION OF HEMODIALYSIS VASCULAR ACCESS STENOSISR01HL067646 · NHLBI · UNIVERSITY OF UTAH · PI CHEUNG, ALFRED K · 2002 to 2010
$8.0M
Hemodynamics and Vascular Wall Biology Determine Arteriovenous Fistula MaturationR01DK088777 · NIDDK · UNIVERSITY OF UTAH · PI BERCELI, SCOTT A, CHEUNG, ALFRED K · 2011 to 2014
$2.6M
NHLBI NIH HHS R01 HL067646NIDDK NIH HHS R01 DK088777
6 · The paper itself

Abstract

Surgically-created blood conduits used for chronic hemodialysis, including native arteriovenous fistulas (AVFs) and synthetic AV grafts (AVGs), are the lifeline for kidney failure patients. Unfortunately, each has its own limitations: AVFs often fail to mature to become useful for dialysis and AVGs often fail due to stenosis as a result of neointimal hyperplasia, which preferentially forms at the graft-venous anastomosis. No clinical therapies are currently available to significantly promote AVF maturation or prevent neointimal hyperplasia in AVGs. Central to devising strategies to solve these problems is a complete mechanistic understanding of the pathophysiological processes. The pathology of arteriovenous access problems is likely multi-factorial. This review focuses on the roles of fluid-wall shear stress (WSS) and endothelial cells (ECs). In arteriovenous access, shunting of arterial blood flow directly into the vein drastically alters the hemodynamics in the vein. These hemodynamic changes are likely major contributors to non-maturation of an AVF vein and/or formation of neointimal hyperplasia at the venous anastomosis of an AVG. ECs separate blood from other vascular wall cells and also influence the phenotype of these other cells. In arteriovenous access, the responses of ECs to aberrant WSS may subsequently lead to AVF non-maturation and/or AVG stenosis. This review provides an overview of the methods for characterizing blood flow and calculating WSS in arteriovenous access and discusses EC responses to arteriovenous hemodynamics. This review also discusses the role of WSS in the pathology of arteriovenous access, as well as confounding factors that modulate the impact of WSS.

Indexed as

Arteriovenous fistulaArteriovenous graftsEndothelial cellsHemodialysis vascular accessHemodynamicsShear stress

Identifiers

PMID25309636
PMCPMC4189833
OpenAlexW2163721602

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.