The natural history of autogenous radio-cephalic wrist arteriovenous fistulas of haemodialysis patients: a prospective observational study.

BACKGROUND: Clinical practice guidelines have supported vascular access surveillance programmes on the premise that the natural history of the vascular access will be altered by radiological or surgical interventions after vascular access dysfunction is detected. The primary objective of this study was to assess the actual risk of thrombosis of autogenous radio-cephalic (RC) wrist arteriovenous fistulas (AVFs) without any pre-emptive interventions. METHODS: We enrolled 52 randomly selected adult Caucasian prevalent haemodialysis (HD) patients, all with autogenous RC wrist AVFs, into this prospective, observational study aimed to follow the natural history of their AVFs for 4 years. The protocol prescribed avoiding any surgical or interventional radiological procedures until access failure (AVF thrombosis or a vascular access not assuring a single-pool Kt/V > or =1.2). The subjects underwent yearly assessments of vascular access blood flow rate by means of a saline ultrasound dilution method. RESULTS: All failures of vascular access were due to AVF thrombosis; none were attributed to an inadequacy of the dialysis dose. AVF thrombosis occurred in nine cases; a rate of 0.043 AVF thrombosis per patient-year at risk. A receiver operating characteristic curve, evaluating the diagnostic accuracy of baseline vascular access blood flow rate values in predicting AVF failure, showed an under-the-curve area of 0.82+/-0.05 SD (P = 0.01). The value of vascular access blood flow rate, identified as a predictor of AVF failure, was <700 ml/min with an 88.9% sensitivity and 68.6% specificity. When subdividing the population of AVFs into two groups according to the baseline vascular access blood flow rates, two out of the nine thromboses occurred among the AVFs that had baseline blood flow rates >700 ml/min (n = 31), whereas seven occurred among the AVFs that had baseline blood flow rates <700 ml/min (n = 21). The 4 year cumulative actuarial survival was 74.36 and 20.80%, respectively (log-rank test, P = 0.04). The 24 AVFs that remained patent at the end of the 4 years maintained a median blood flow rate > or =900 ml/min at all time points studied. Worth noting is that, five of them (20.8%) remained patent throughout the study with a blood flow rate consistently < or =500 ml/min. CONCLUSIONS: This study shows a very low rate of AVF thrombosis per patient-year at risk and a high actuarial survival of autogenous RC wrist AVFs, particularly of those having a blood flow rate >700 ml/min. Thus, a vascular access blood flow rate <700 ml/min appears to be a reliable cut-off point at which to start a closer monitoring of this parameter-which may lead to further investigations and possibly interventions relevant to the function of the AVFs.

Hyperbaric oxygen therapy for calcific uremic arteriolopathy: a case series.

Calcific uremic arteriolopathy (CUA), also referred to as calciphylaxis, is a syndrome of small vessel calcification of unknown etiology causing painful violaceous skin lesions that progress to non-healing ulcers and gangrene. It is observed mainly in patients with end-stage renal disease, is associated with high morbidity and mortality and has no standard treatment at the present time. Although parathyroidectomy (PTX) has been advocated in some cases, other studies have not found this effective. Hyperbaric oxygen therapy (HOT) consists of breathing 100% O2 at higher than ambient pressure, with the patient inside a sealed chamber. HOT has been used with some success in the treatment of selected problem wounds (those that fail to respond to established medical and surgical management). They are often severely hypoxic; restoration of tissue PO2 to normal or above-normal enhances fibroblast proliferation and collagen production as well as angiogenesis. The present is the largest retrospective case series of CUA treated by means of HOT reported so far and comprises 11 chronic uremic patients on dialysis (9 hemo- and 2 peritoneal dialysis, 6 females and 5 males, mean age 56 +/- 7 SD years, time on dialysis 163 +/- 84 SD months). Four patients had biopsy-proven CUA; 3 had diabetic nephropathy as a cause of uremia; 2 were obese and 3 had a consistent increase of serum calcium x phosphorus product; 3 patients had severe secondary hyperparathyroidism (II(nd) HPTH) and two had been submitted to subtotal PTX some years before CUA; two others had already had the limb amputated. Lesions were in the legs, except for one in a hand, and were prevalently ulcers and necrosis. The number of sessions in each HOT cycle ranged from a minimum of 20 to a maximum of 108 (mean 40.6 +/- 29.0). The results of two therapies cannot be evaluated (one was interrupted by the patient after 10 sessions, and one ended with the death of the patient due to ventricular arrhythmia after eight sessions). Eight of the nine remaining had excellent results with healing of the skin ulcers, but the ninth got worse, making it advisable to amputate the foot. In conclusion, CUA appears to result from a multitude of predisposing and/or sensitizing events that are commonly present in the uremic milieu. The specific factors that induce this disorder in an individual patient are not known. The present retrospective study supports a role of HOT in many cases of CUA, especially considering that, in the absence of severe II(nd) HPTH, there are very few therapeutic options.