Indoxyl sulfate, a nephrovascular uremic toxin, is markedly accumulated in the serum of chronic kidney disease (CKD) patients. Because of its protein binding ability, its removal by hemodialysis is not as efficient as that of non-protein bound uremic toxins. AST-120 delays the progression of CKD by adsorbing indole, a precursor of indoxyl sulfate, in the intestines, and consequently reduces the serum levels of indoxyl sulfate. Indoxyl sulfate exhibits cellular toxicity in renal tubular cells, glomerular mesangial cells, vascular smooth muscle cells, vascular endothelial cells, cardiac myocytes, and osteoblasts by inducing oxidative stress. Indoxyl sulfate stimulates the progression of CKD by increasing the expression of fibrogenic genes such as transforming growth factor-β1 in CKD rats. Indoxyl sulfate stimulates aortic calcification in hypertensive rats; thus, indoxyl sulfate is involved in the progression of CKD and cardiovascular disease. Experimental and clinical data demonstrate that AST-120 delays the progression not only of chronic kidney disease, but also of cardiovascular disease.
© 2011 The Author. Therapeutic Apheresis and Dialysis © 2011 International Society for Apheresis.