Effect of the veins histopathological characteristics and preexisting medical conditions on arteriovenous fistula maturation and primary patency in patients with end-stage renal disease: an observational, prospective study.

We assessed the veins histopathological characteristics and preexisting medical conditions before arteriovenous fistula (AVF) creation, and their correlation with AVF outcome and primary patency in patients with end-stage renal disease (ESRD). In this observational, prospective, mono-center study in Romania, patients with artery and venous diameters =2 mm and =2.5 mm, respectively, were enrolled. Vein specimens were harvested at AVF creation and evaluated by Hematoxylin and Eosin, Masson's trichrome and Orcein stainings, in terms of intimal hyperplasia, elastic fibers disposition, medial hypertrophy and smooth muscle cell disorganization and fibrosis (graded from mild to severe). Venous diameters and blood flow one÷two-months post-AVF creation, AVF maturation at dialysis start, two-year primary patency were assessed. Of 115 examined patients, 50 were enrolled and underwent AVF creation. Of six (12%) patients with no vein morphological changes, 11 (22%) with mild histopathological changes, 19 (38%) with moderate and 14 (28%) with severe histopathological changes, four (67%), eight (73%), 17 (89%) and 12 (86%), respectively, had mature AVF. Regardless of histopathological characteristics, non-mature AVF were recorded in older patients and with smaller venous diameter. One÷two-months post-AVF creation, in all patients with mature AVF, venous diameter and ultrasonographic blood flow were similar. Two years post-AVF creation, 26 patients had functional AVF; non-functional AVFs were recorded more likely in women and functional AVFs were most likely located on forearm. The veins histopathological modifications may not negatively influence AVF maturation in ESRD patients. AVF maturation failure may most likely be related to age and venous diameter at AVF creation.

Matrix-Metalloproteinase-2 Predicts Arteriovenous Fistula Failure in Hemodialysis Patients.

In hemodialysis patients the principal cause of arteriovenous fistula dysfunction is stenosis. Matrix-metalloproteinase-2 is implicated in the pathophysiological mechanism of stenosis development. Our study tried to assess the clinical impact of this protease on arteriovenous fistula survival. Seventy-nine prevalent dialysis patients with functional arteriovenous fistulas were included in the study. The presence of stenosis and the serum levels of matrix-metalloproteinase-2 were determined at the beginning of the study. The patency of the arteriovenous fistulas was followed- up for two years. In multivariate regression; matrix-metalloproteinase-2 was a significant predictor of vascular access loss (HR = 1.104, 95%CI 1.033-1.179, P = 0.003). Patients with a level of matrix-metalloproteinase-2 lower than 50 ng/mL had a better survival of the arteriovenous fistulas. Matrix-metalloproteinase-2 was an even stronger predictor of fistula failure in the stenosis group (HR = 1.076, 95%CI 1.027-1.127, P = 0.002). In our study matrix-metalloproteinase-2 has a predictive value for arteriovenous fistula failure.

Relationship of adiponectin to markers of oxidative stress in type 2 diabetic patients: influence of incipient diabetes-associated kidney disease.

PURPOSE: Adiponectin may be beneficial in incipient chronic kidney disease by antagonizing oxidative stress. We evaluated adiponectin, malondialdehyde (MDA), and superoxide dismutase (SOD), in type 2 diabetes mellitus patients (T2DP) with and without incipient nephropathy. METHODS: T2DP with glomerular filtration rate (GFR) >30 ml/min were compared with 20 healthy controls. Clinical and laboratory evaluations, levels of MDA (fluorimetric thiobarbituric test), SOD (cytochrome reduction method) and adiponectin (ELISA) were obtained. RESULTS: Sixty-four patients (GFR 91.44 ± 38.50 ml/min, urinary albumin-to-creatinine ratio [UACR] 20.81 [4.64-72.88 mg/g]) were included. MDA was higher in T2DP than in controls: 3.97 (2.43-4.59) versus 1.35 (1.16-1.81) nmol/ml, p < 0.0001. MDA correlated with glycated hemoglobin (r = 0.40, p = 0.001), adiponectin (r = -0.28, p = 0.03), systolic blood pressure (r = -0.28, p = 0.03) and SOD (r = -0.35, p = 0.005); adiponectin (p = 0.01) and glycated hemoglobin (p = 0.02) remained significant predictors of MDA in multiple regression analysis. SOD was negatively correlated with glycemia (r = -0.71, p < 0.0001) and glycated hemoglobin (r = -0.5, p < 0.0001). When patients were divided according to a ROC-derived adiponectin cutoff of 8.9 µg/ml, patients with higher adiponectin had lower MDA, [2.55 (2.35-3.60) vs. 4.10 (2.89-5.31) nmol/ml, p = 0.005] but similar SOD levels. In T2DP with nephropathy (GFR < 60 ml/min or UACR > 30 mg/g), the correlation of adiponectin with MDA was stronger, (r = -0.51, p = 0.004) confirmed in multiple regression analysis (p = 0.03). Adiponectin was not correlated with MDA, and SOD was inversely related to MDA in patients without nephropathy. CONCLUSION: Adiponectin is a significant predictor of MDA in early diabetic nephropathy, whereas SOD strongly depends only on glycemic control and is not directly related to adiponectin.