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• W2079726360 abstract "There is renewed interest in chronic kidney disease (CKD) as an underlying risk factor for the development of cardiovascular disease. Not only end-stage renal failure, but also proteinuria and mild reduction of glomerular filtration have been shown to be independent risk factors for cardiovascular disease and factors that adversely affect outcomes [ [1] de Zeeuw D. Remuzzi G. Parving H.H. Keane W.F. Zhang Z. Shahinfar S. et al. Albuminuria, a therapeutic target for cardiovascular protection in type 2 diabetic patients with nephropathy. Circulation. 2004; 110: 921-927 Crossref PubMed Scopus (682) Google Scholar ]. Indoxyl sulfate, a uremic toxin, may play an important role in endothelial dysfunction via generation of oxidative stress and induction of endothelial senescence [ [2] Yu M. Kim Y.J. Kang D.H. Indoxyl sulfate-induced endothelial dysfunction in patients with chronic kidney disease via an induction of oxidative stress. Clin J Am Soc Nephrol. 2011; 6: 30-39 Crossref PubMed Scopus (243) Google Scholar ]. In addition, indoxyl sulfate may be a valuable predictor of vascular disease. A higher mortality rate was observed in CKD patients with higher serum indoxyl sulfate levels [ [2] Yu M. Kim Y.J. Kang D.H. Indoxyl sulfate-induced endothelial dysfunction in patients with chronic kidney disease via an induction of oxidative stress. Clin J Am Soc Nephrol. 2011; 6: 30-39 Crossref PubMed Scopus (243) Google Scholar ]. One study demonstrated that indoxyl sulfate had pro-fibrotic, pro-hypertrophic, and pro-inflammatory effects, indicating that indoxyl sulfate may play an important role in adverse cardiac remodeling, mediated via activation of the p38 MAPK, p42/44 MAPK, and nuclear factor (NF)-κB pathways [ [3] Lekawanvijit S. Adrahtas A. Kelly D.J. Kompa A.R. Wang B.H. Krum H. Does indoxyl sulfate, a uraemic toxin, have direct effects on cardiac fibroblasts and myocytes?. Eur Heart J. 2010; 31: 1771-1779 Crossref PubMed Scopus (250) Google Scholar ]. Targeting reduction of indoxyl sulfate and/or inhibition of its activation pathways may represent a novel therapeutic approach to the management of cardiovascular disease with concomitant CKD. AST-120 (Kremezin®) suppresses the progression of CKD by absorbing and removing a precursor of uremic toxin produced in the intestinal tract, and is the only agent with an indication for “improving uremic symptoms in chronic kidney disease and prolonging the initiation of dialysis” [ [4] Akizawa T. Asano Y. Morita S. Wakita T. Onishi Y. Fukuhara S. et al. on behalf of the CAP-KD study group. Effect of a carbonaceous oral adsorbent on the progression of chronic kidney disease: a multicenter, randomized, controlled trial. Am J Kidney Dis. 2009; 54: 459-467 Abstract Full Text Full Text PDF PubMed Scopus (137) Google Scholar ]. However, only a few reports have evaluated the effects of AST-120 on both indoxyl sulfate and oxidative stress simultaneously in a clinical setting. This study was designed to evaluate the impact of AST-120 on indoxyl sulfate levels, d-ROMs (a marker of oxidative stress), renal function markers, and other biomarkers." @default.
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• W2079726360 date "2014-12-01" @default.
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• W2079726360 title "Impact of the oral adsorbent AST-120 on oxidative stress and uremic toxins in high-risk chronic kidney disease patients" @default.
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• W2079726360 doi "https://doi.org/10.1016/j.ijcard.2014.09.196" @default.
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