A well-functioning vascular access (VA) is a mainstay to perform an efficient hemodialysis (HD) procedure. There are three main types of access: native arteriovenous fistula (AVF), arteriovenous graft, and central venous catheter (CVC). AVF, described by Brescia and Cimino, remains the first choice for chronic HD. It is the best access for longevity and has the lowest association with morbidity and mortality, and for this reason AVF use is strongly recommended by guidelines from different countries. Once autogenous options have been exhausted, prosthetic fistulae become the second option of maintenance HD access alternatives. CVCs have become an important adjunct in maintaining patients on HD. The preferable locations for insertion are the internal jugular and femoral veins. The subclavian vein is considered the third choice because of the high risk of thrombosis. Complications associated with CVC insertion range from 5% to 19%. Since an increasing number of patients have implanted pacemakers and defibrillators, usually inserted via the subclavian vein and superior vena cava into the right heart, a careful assessment of risk and benefits should be taken. Infection is responsible for the removal of about 30%–60% of HD CVCs, and hospitalization rates are higher among patients with CVCs than among AVF ones. Proper VA maintenance requires integration of different professionals to create a VA team. This team should include a nephrologist, radiologist, vascular surgeon, infectious disease consultant, and members of the dialysis staff. They should provide their experience in order to give the best options to uremic patients and the best care for their VA.
A wide array of immune cells, including lymphocytes, is known to be present and to play a pathogenetic role in atherosclerotic lesions. However, limited information is currently available regarding the presence of Natural Killer (NK) cell subsets within vessel plaque, and more in general, regarding their role in human atherosclerosis. We evaluated the distribution of NK cells in human carotid atherosclerotic plaques, dissecting asymptomatic and symptomatic patients (identified as affected by stroke, transient ischemic attack, or amaurosis fugax within 6 months) with the aim of shedding light on the putative contribution of NK cells to the pathogenic process that leads to plaque instability and subsequent clinical complications. We observed that carotid plaques were consistently infiltrated by NK cells and, among them, CD56
bright
perforin
low
NK cells were abundantly present and displayed different markers of tissue residency (i.e., CD103 CD69 and CD49a). Interestingly, carotid atherosclerotic plaques of symptomatic patients showed a higher content of NK cells and an increased ratio between CD56
bright
perforin
low
NK cells and their CD56
dim
perforin
high
counterpart. NK cells isolated from plaques of symptomatic patients were also stronger producers of IFN-γ. Analysis of the expression of NK activating receptor ligands (including MICA/B, ULBP-3, and B7-H6) in atherosclerotic carotid plaques revealed that they were abundantly expressed by a HLA-DR
+
CD11c
+
myeloid cell population resident in the plaques. Remarkably, sera of symptomatic patients contained significant higher levels of soluble ligands for NK activating receptors. Our observations indicate that CD56
bright
NK cells accumulate within human atherosclerotic lesions and suggest a possible contribution of NK cells to the process determining plaque instability.
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