Abstract
Chronic kidney disease (CKD) has been considered a major risk factor for cardiovascular diseases. Although great advances have recently been made in the pathophysiology and treatment of cardiovascular diseases, CKD remains a major global health problem. Moreover, the occurrence rates of cardiovascular events among CKD patients increase even in cases in which patients undergo hemodialysis, and the mechanisms underlying the so-called “cardiorenal syndrome” are not clearly understood. Recently, small-molecule uremic toxins have been associated with cardiovascular mortality in CKD and/or dialysis patients. These toxins range from small uncharged solutes to large protein-bound structures. In this review, we focused on protein-bound uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, which are poorly removed by current dialysis techniques. Several studies have demonstrated that protein-bound uremic toxins, especially indoxyl sulfate, induce vascular inflammation, endothelial dysfunction, and vascular calcification, which may explain the relatively poor prognosis of CKD and dialysis patients. The aim of this review is to provide novel insights into the effects of indoxyl sulfate and p-cresyl sulfate on the pathogenesis of atherosclerosis.
Highlights
Cardiovascular death is approximately 10–20 times more frequent in dialysis patients than in healthy individuals [1], owing to a high prevalence of coronary artery diseases in this population [2].Even in patients with mild-to-moderate chronic kidney disease (CKD), the estimated glomerular filtration rate is inversely correlated with the development of cardiovascular disease and mortality [3]
We focused on protein-bound uremic toxins that are poorly removed by current dialysis techniques because of their size, which is larger than the pore size of dialysis membranes [9]
The aim of this review is to provide novel insights into the effects of indoxyl sulfate and p-cresyl sulfate on the pathogenesis of atherosclerosis
Summary
Even in patients with mild-to-moderate chronic kidney disease (CKD), the estimated glomerular filtration rate (eGFR) is inversely correlated with the development of cardiovascular disease and mortality [3]. Keith et al showed that in CKD patients, death occurred even before the patients had the opportunity to receive renal replacement therapy [4]. Prevention of cardiovascular disease (CVD) is critical for patients with renal dysfunction. Traditional risk factors, such as age, diabetes, and hypertension, as well as non-traditional risk factors, such as uremic toxins, anemia, and Ca/P abnormalities, play central roles in the pathogenesis of atherosclerosis in patients with renal disease [5,6]. In spite of advances in therapeutic approaches for kidney complications, such as anemia and Ca/P imbalance, the therapeutic strategies aimed at reducing the amounts and effects of uremic toxins remain insufficient
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