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Effect of Arteriovenous Fistula Creation on Systolic and Diastolic Blood Pressure in Patients With Pre-dialysis Advanced Chronic Kidney Disease.

ABSTRACT:

Background

Central arteriovenous fistula (cAVF) has been investigated as a therapeutic measure for treatment-resistant hypertension in patients without advanced chronic kidney disease (CKD). There is considerable experience with the use of AVF for hemodialysis in patients with end-stage renal disease (ESRD). However, there is sparse data on the blood pressure (BP) effects of an AVF among patients with ESRD. We hypothesized that AVF creation would significantly reduce BP compared with patients who did not have an AVF among patients with ESRD before starting hemodialysis.

Methods

BPs were compared during the 12 months before hemodialysis initiation in 399 patients with an AVF or AV graft created and 4,696 patients without either.

Results

After propensity score matching 1:2 ratio (AVF to no AVF), repeated measures analysis of variance revealed significant reductions of -1.7 mm Hg systolic and -3.9 mm Hg diastolic BP 12 months in patients after AVF creation; P = 0.025 and P < 0.001, respectively, compared with those with no AVF.

Conclusions

These findings suggest that AVF creation results in modest BP reduction in patients with pre-dialysis ESRD who require AVF for eventual hemodialysis therapy. Preferential diastolic BP reduction suggests that greater work is needed to characterize the ideal patient subset in which to use cAVF for treatment-resistant hypertension in those without advanced CKD.

SUBMITTER: Mathew RO

PROVIDER: S-EPMC6937624 | biostudies-literature |

REPOSITORIES: biostudies-literature

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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.