Factors influencing dialysis arteriovenous graft survival.

PURPOSE: Dysfunction and loss of patency of dialysis arteriovenous grafts (AVGs) are serious causes of morbidity in patients on dialysis. Various risk factors associated with shorter AVG patency have been blamed, but the results of the studies were controversial. The aim of this study was to assess if associated diseases, biochemical markers and other parameters associated with atherosclerosis influence patency of AVGs in a large vascular access centre. METHODS: We conducted a retrospective study that included patients with AVGs patent for at least 3 weeks after creation. We included variables associated with atherosclerosis into the analysis (coronary artery disease, diabetes mellitus, chronic heart failure, arterial hypertension, smoking history and cholesterol and triglyceride levels) and characteristics of the graft (shape, feeding artery).The data was assessed using log-rank (Cox-Mantel) test. The differences were shown using Kaplan-Meier graphs. The observation period was limited to 1000 days after access creation. RESULTS: Overall, 338 patients were included in the study. Significantly higher risk of access failure was associated with presence of coronary artery disease (p = 0.0035). Higher serum cholesterol levels were associated with longer survival of the graft in 1000 days of surveillance (p = 0.04). CONCLUSIONS: Coronary artery disease negatively influences the cumulative patency of vascular access. Higher serum cholesterol levels are associated with lower AVG failure risk over a 1000-day period, which probably corresponds to the worse disease status of the patients with lower cholesterol values.

Arteriovenous grafts: early ultrasonography tells their fortune.

BACKGROUND: The patency of arteriovenous grafts (AVG) for hemodialysis is mostly limited by growing stenoses that lead to decreasing of blood flow, thromboses and finally to access failure. The aim of this study was to find out if detection of any pathology by duplex Doppler ultrasonography (DDU) early after creation of AVG could identify those with lower survival. METHODS: We retrospectively enrolled AVG examined by DDU in our center within 40 days after their creation during the last 10 years. The findings were divided into 4 subgroups: (1a) normal finding, (1b) DDU risk factor (low flow volume, medial calcinosis of the feeding artery, presence of intimal hyperplasia in the venous anastomosis), (2a) non-significant or (2b) significant stenosis. The primary outcome measure was the cumulative survival of people with AVGs, and the secondary was the primary (unassisted) survival. All patients underwent DDU surveillance every 3 months with pre-emptive treatment of significant stenoses. RESULTS: Overall, 340 cases were found; the median follow-up was 565 days. Normal DDU finding had 60% cases, DDU risk factor 18% cases, non-significant stenosis 13% cases and significant stenosis 9% cases. Occurrence of early significant stenosis was associated with high risk of access loss (hazards ratio (HR) 14.73; 95% CI 5.10-42.58; p < 0.0001). Similarly, the presence of a DDU risk factor and of a non-significant stenosis were related to significantly shorter access lifespan (HR 2.86; 95% CI 1.10-7.40; p = 0.03 and HR 2.83; 95% CI 1.12-7.17; p = 0.03, respectively). CONCLUSION: DDU examination of AVG early after their creation can identify those at higher risk and may contribute to individualize the surveillance strategy.

The effect of coenzyme Q10 in statin myopathy.

OBJECTIVES: Statins significantly reduce CV morbidity and mortality. Unfortunately, one of the side effects of statins is myopathy, for which statins cannot be administered in sufficient doses or administered at all. The aim of this study was to demonstrate the effect of coenzyme Q10 in patients with statin myopathy. DESIGN/SETTING: Twenty eight patients aged 60.6±10.7 years were monitored (18 women and 10 men) and treated with different types and doses of statin. Muscle weakness and pain was monitored using a scale of one to ten, on which patients expressed the degree of their inconvenience. Examination of muscle problems was performed prior to administration of CQ10 and after 3 and 6 months of dosing. Statistical analysis was performed using Friedman test, Annova and Students t-test. RESULTS: Pain decreased on average by 53.8% (p<0.0001), muscle weakness by 44.4% (p<0.0001). The CQ10 levels were increased by more than 194% (from 0,903 µg/ml to 2.66 µg/ml; p<0.0001). CONCLUSION: After a six-month administration of coenzyme Q10, muscle pain and sensitivity statistically significantly decreased.

Effect of folic acid on fenofibrate-induced elevation of homocysteine and cysteine.

BACKGROUND: An elevated total plasma homocysteine (tHcy) level is considered to be an independent risk factor for atherosclerosis. It has been reported that lipid-lowering therapy with fibric acid derivatives (fibrates) increases tHcy and total plasma cysteine (tCys) levels. The aim of this study was to determine whether therapy with folic acid, a potent tHcy-lowering agent, could modify the fenofibrate-induced elevation of plasma aminothiols. METHODS: Patients with combined hyperlipidemia (n = 37) were randomized to receive 9 weeks of treatment with micronized fenofibrate 200 mg/day (F group) or fenofibrate 200 mg/day plus folic acid 10 mg/every other day (F+F group). tCys and tHcy levels were determined before and after the therapy with high performance liquid chromatography. RESULTS: The tHcy level increased significantly in the F group by 51.3% and in the F+F group by 14.6% (between-group difference P =.001). Total plasma cysteine (tCys) increased similarly after both treatments (P =.72). The serum creatinine level increased in the F group by 20.7% and in F+F group only by 9.8% (P =.04). The increase of tHcy level in F group correlated with an increase of tCys and creatinine levels (r = 0.74 and 0.64, respectively). The effects on the lipid profile did not differ by treatment group. CONCLUSIONS: Folic acid effectively reduces the fenofibrate-induced elevation of tHcy and creatinine, but it does not affect the elevation of the tCys. Folic acid has neutral effect on the lipid-lowering action of fenofibrate. Clinical efficacy of fenofibrate might be improved by folic acid coadministration.