Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genes differently expression between human failed arteriovenous fistula (AVF) and the control

ABSTRACT: From January 1, 2018 to December 31, 2018, there were 19 patients (from four hemodialysis centers) undergoing failing arteriovenous fistula (AVF) that were resistant to endovascular therapy with extensive fistula aneurysmal change (n=4), diffuse stenosis (n=13) or poor skin condition of the forearm (n=2). While 13 of them manifested good size and quality of the outflow vein (>10 cm long, >6 mm in diameter and <6 mm under the skin, BF >600 ml/min) to create of a new AVF upstream. They have been provided with an end-to-side anastomosis of the outflow vein with the more proximal inflow artery, together with ligation of the failing downstream AVF. During the operation, the small segment adjacent to the distal healthy access was exercised for the control access (CA) sample. Until December 31, 2019, 5 of 13 patients had suffered failing AVF again, followed by the excision of segment of high-grade stenosis for the failing access (FA) samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Yang Yang

PROVIDER: E-MTAB-15287 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:In patients with severe kidney disease AVF are surgically placed in order to create good access for hemodialysis. In these dialysis patients the failure rates of AVF can be as high as 24% within 6 months after surgery, causing ineffective dialysis and necessitating additional clinical interventions. The pathological processes known to lead to AVF failure are beginning to be unravelled include the formation of venous neointimal hyperplasia (VNIH), thrombosis (Chang et al. PMID 16105066), and venous stenosis (Kanterman et al. PMID7892454, Tang et al. 1998), resulting in a reduced blood flow through the fistula. We established a rat model for AVF failure in human kidney dialysis patients. The characterization of this model has been previously described (Globerman et al. 2011, PubmedID:22002501). In this model the AVFs are surgically constructed in the right leg by connecting the superficial epigastric vein SEV to the common femoral artery (CFA), resulting in exposure of the SEV to arterial pressure with pulsatile and low resistant flow patterns (Globerman et al. 2011, PMID22002501). In the present study we utilized this AVF model in order to assess the effects of arterialized flow, with consequent pathological changes of the vessel wall due to surgical AVF instalment, on the transcriptome of endothelium from the SEV. Within the SEV these pathologies of the vessel wall include the formation of NIH in the main branch, and stenosis in the side branches. By employing this rat model we assessed the changes of the endothelial transcriptome in relation to these pathologies in order to gain mechanistic understanding of the potential roles of venous endothelium in AVF failure, as well as to identify potential biomarkers preceding AVF failure. AVF surgery was performed on N=6 rats, and 13-14 days after surgery the rats were sacrificed. AVFs were extracted from the rats, and microarray transcriptome analyses were performed on luminal endothelial cells that isolated from four different sites of the AVF by employing Laser Capture Microdissection (LCM). These sites included (i) N=5 AVF sections of the superficial epigastric vein (SEV) with neointimal hyperplasia (NIH), (ii) N=3 AVF sections of SEV side branches with luminal stenosis, (iii), N=6 sections of the SEV located distally from a ligation thereby omitting exposure to arterialized flow and consequently preventing the development of NIH or stenosis, and (iv) N=3 sections of the AVF common femoral artery without signs of NIH or stenosis.

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Genes differently expression between human failed arteriovenous fistula (AVF) and the control

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