Abstract
Patients with chronic kidney disease (CKD) have an increased risk of vascular disease, which is associated with considerable health care costs. Vascular disease in CKD differs clinically and pathobiologically from that in patients with normal renal function. Besides the traditional risk factors, retention of uremic toxins contributes to the pathogenesis of vascular disease in patients with CKD. Indoxyl sulfate is a protein-bound uremic toxin and is inefficiently removed by conventional dialysis. Accumulating evidence suggests that indoxyl sulfate is a vascular toxin involved in atherosclerosis, arteriosclerosis, vascular calcification and vascular repair. Clinically, indoxyl sulfate is associated with total and cardiovascular mortality in patients with CKD. Recent studies have indicated that in addition to coronary and cerebral arteries, indoxyl sulfate plays a role in peripheral artery disease (PAD) and dialysis graft thrombosis. Emerging evidence suggests that indoxyl sulfate is implicated via novel mechanisms, including progenitor cell-related neovascularization and tissue factor-related hypercoagulability. These findings raise the possibility that strategies targeting serum indoxyl sulfate may have the potential to improve the outcomes of PAD and dialysis vascular access in patients with CKD.
Highlights
Dysfunction of dialysis vascular accesses continues to be a major source of morbidity and mortality in patients with end-stage renal disease (ESRD)
We focus on the effect of indoxyl sulfate on the angiogenesis of peripheral artery disease (PAD) and thrombosis of dialysis vascular accesses
These findings suggest that indoxyl sulfate may contribute to the progression of atherosclerosis in patients with chronic kidney disease (CKD) by inducing inflammation and endothelial dysfunction
Summary
Compared to patients with preserved kidney function, patients with chronic kidney disease (CKD). Vascular disease-related ischemic events cause significant morbidity and mortality in patients with CKD [1]. An increased risk of myocardial infarction and ischemic stroke has been widely reported in patients with CKD [1,2,3,4,5,6]. Creation of vascular accesses for dialysis, including native arteriovenous. Traditional vascular risk factors are common in patients with CKD, they cannot sufficiently account for the increased vascular events [2]. Understanding the unique pathophysiology of vascular disease in patients with CKD may help to develop strategies for prevention and therapy. We will focus on the novel mechanisms of the effect of indoxyl sulfate on PAD and dialysis vascular accesses
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