Influence of cephalic vein dilation on arteriovenous fistula maturation in patients with small cephalic veins.

A substantial limitation of dialysis fistulas is their high primary failure rate due to nonmaturation. Various studies have documented that patients with larger vein diameters exhibit reduced risks for nonmaturation. Nevertheless, some patients have small veins. Few studies have focused on patients with small veins. We hypothesize that sufficient venous dilation contributes to fistula maturation. Therefore, we studied the influence of cephalic vein dilation on fistula maturation in patients with small veins.Patients with small cephalic veins (diameter <2 mm) undergoing initial arteriovenous fistulae (AVF) operation were included. A total of 72 patients were enrolled in this study. A prospective study was performed, and the patients were followed for 6 weeks after surgery. Preoperative and postoperative duplex ultrasound mapping of veins was performed, and dilation of the cephalic vein was evaluated.The fistula maturation rate was 44.44%. Multivariate logistic regression analysis revealed a significant relationship between fistula maturation and preoperative cephalic vein dilation. Based on the results of ROC analysis, the fistula maturation rate in patients with vein dilation greater than or equal to the cut-off was 57.14% in the training data set and 54.55% in the testing data set. The independent influencing factors for fistula maturation were used to establish a combined index with logistic regression analysis. The fistula maturation rate in patients with combined indexes greater than or equal to the cut-off was 80.95% in the training data set and 77.78% in the testing data set.Our results demonstrated that preoperative venous dilation was associated with AVF maturation. For patients with small veins, venous distensibility needs to be carefully assessed before surgery, as it may be a better predictor of AVF maturation than venous diameter.

Influence of blood pressure variability on the life of arteriovenous fistulae in maintenance hemodialysis patients.

BACKGROUND: Although numerous risk factors for arteriovenous fistulae (AVF) dysfunction have been identified, these risk factors do not explain all cases of AVF dysfunction. Because of the importance of blood pressure variability (BPV) in vascular injury, the predictive value of BPV for AVF dysfunction, was evaluated in this prospective cohort study. METHODS: Twenty-four-hour BP monitoring at the intervals of dialysis was recorded every 3 months in 137 patients. The expression of smooth muscle actin (SMA) and the infiltration of mononuclear cells and T lymphocytes were determined by immunohistochemistry on the specimens of fistula vessels. RESULTS: Eighteen patients developed AVF dysfunction. Cox proportional hazards multivariate analysis revealed a significant relationship between fistula dysfunction and daytime systolic-BPV (d-SBPV), nighttime systolic-BPV (n-SBPV), diabetes mellitus, and initial venous diameter. Patients with AVF dysfunction were observed to have increased SMA expression and more infiltration of inflammatory cells in venous walls compared with the controls. A significant correlation between SBPV and the infiltration of CD68-positive cells was observed. CONCLUSIONS: Our study showed that the degrees of SBPV were significantly associated with the risk of AVF dysfunction. Potentially, the increase of SBPV will aggravate venous wall inflammation and may play a role in AVF dysfunction.

MicroRNA-33 suppresses CCL2 expression in chondrocytes.

CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully elucidated. In the present study, we demonstrated that the binding sites of miR-33 in the 3'UTR of CCL2 gene were conserved in human, mouse and rat species. By performing gain- or loss-of-function studies, we verified that miR-33 suppressed CCL2 expression in the mRNA and protein levels. We also found that miR-33 suppressed the CCL2 levels in the supernatant of cultured primary mouse chondrocytes. With reporter gene assay, we demonstrated that miR-33 targeted at AAUGCA in the 3'UTR of CCL2 gene. In transwell migration assays, we demonstrated that the conditional medium (CM) from miR-33 deficient chondrocytes potentiated the monocyte chemotaxis in a CCL2 dependent manner. Finally, we demonstrated that the level of miR-33 was decreased, whereas the CCL2 level was increased in the articular cartilage from the OA patients compared with the control group. In summary, we identified miR-33 as a novel suppressor of CCL2 in chondrocytes. The miR-33/CCL2 axis in chondrocytes regulates monocyte chemotaxis, providing a potential mechanism of macrophage infiltration in OA.