Thrombosis of the vascular access (CA) is usually due to technical problems and/or small arterial or venous size, obesity, advanced age, diabetes mellitus, female sex and AVF in the wrist.

We present a case, not previously described, of early AVF thrombosis secondary to paradoxical embolism caused by a patent foramen ovale (PFO). He is an 80-year-old man; after 7 years in PD is switched to because of poor dose of dialysis. A left humerus-perforan vein AVF was made that quickly thrombosed at 24h. During Re-intervention it was observed permeable vessels and a thrombus are detected in the middle third of the humeral artery suggesting an arterial embolism. Thromboembolectomy was successful and anticoagulation was prescribed. The ECG presented sinus rhythm and the echocardiography showed no abnormalities. Transesophageal echocardiography (TEE) is performed, showing PFO with early bubbles after the injection of agitated saline solution. In the descending thoracic aorta, a giant fibrocalcified atherosclerosis plaque with irregularities and thrombotic content occupying 40% of the light was observed.

Thereafter he presented transient cerebrovascular event with loss of intellectual abilities with lower limb chronic small vessel ischemia and injuries suggestive of cholesterol crystals atheroembolism which caused with severe pain, livedo reticularis, cyanotic punctate lesions and cyanosis of the first toe of the left foot with preserved pulses. Then, Sintrom® was discontinued and it was changed to subcutaneous LMWH 60mg/24h, aspirin and clopidogrel were added and statins dose was increased to 80mg daily as recommended by vascular surgery. The patients lost 15kg in 8 months, albumin 2.1g/L and CRP was 57mg/L with severe anemia despite increased EPO. The patient decided to voluntarily stop HD

Paradoxical embolism as the cause of AV thrombosis has not previously been described in the literature. Arterial embolism is a rare cause of fistula thrombosis,1 and even less frequent is paradoxical embolism,2 which is the passage of a venous thrombus located in the right cardiac cavities to the arterial circulation through a cardiac defect. The most frequent is PFO, with a prevalence of 25% by autopsy and 35% by TEE.3

The definitive diagnosis is made if a thrombus going through a septum defect is observed by ultrasound, but a diagnosis also made by: (a) systemic arterial embolism, in the absence of atrial fibrillation, from source located in the left heart cavities or proximal arteries; (b) right-to-left short circuit at any level, and (c) venous thrombosis and/or pulmonary embolism or (d) if PFO is detected, as in the present case.3

Echocardiogram is one of the most useful tools for the diagnosis of emboligial heart disease. With the Valsalva maneuver and the introduction of intravenous contrast a PFO can be identified (sensitivity: 60% and specificity: 78%).3 The diagnostic possibilities improve with TEE.

The treatment of PFO is anticoagulation and, in selected cases, surgical closure or percutaneous closure, with a morbidity of 10%, may be considered.

One important finding in this patient was the presence of a large fibrocalcified atherosclerotic plaque in the descending aorta containing a thrombus. This type of plaques is associated with a high risk of stroke and peripheral embolization.4 In renal patients abdominal aorta calcification is observed in 81% of patients and it is severe in 51% of cases.5 Vascular calcification is an independent risk factor for cardiovascular mortality. These plaques are the cause of 2 types of emboli: thromboembolism and atheroemboli (emboli by cholesterol crystals). The latter are characterized by the release of small emboli either spontaneously (25%) or provoked by interventions such as cardiac catheterization, arteriography, peripheral interventions, or cardiac surgery.6 In this case, the fistula intervention may have been a precipitating factor.

Mortality in patients with extensive atherosclerotic plaques in the thoracic aorta is 20% at 3 years, cerebrovascular events are observed in 20% of patients, other types of embolic events are seen in 7% and 1% may have cholesterol crystals embolism.6

In patients with atherosclerotic aortic plaques, a high incidence of atheroembolism has been attributed to anticoagulants treatment; however recent randomized clinical trials do not seem to confirm this.7

The treatment includes antithrombotic therapy and statins. Presently is recommended either with aspirin 50–325mg daily or clopidogrel 75mg daily versus the combined treatment8 or warfarin administration.9 There are no data on the use of non-vitamin K dependent oral anticoagulants and therefore they are not recommended.

This case illustrates an exceptional complication of AVF, but given the high frequency of atherosclerosis in HD patients it should be considered.