Abstract
Indoxyl sulfate, a uremic toxin, is accumulated in the serum of chronic kidney disease (CKD) patients. A part of the dietary protein-derived tryptophan is metabolized by intestinal bacteria into indole, which is metabolized to indoxyl sulfate in the liver. Indoxyl sulfate stimulates progression of CKD by increasing expression of fibrogenic genes such as transforming growth factor (TGF)-β1. AST-120 delays the progression of CKD by adsorbing indole in the intestines, and consequently reducing serum 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 reactive oxygen species. Indoxyl sulfate stimulates aortic calcification in hypertensive rats. Thus, indoxyl sulfate is involved in the progression of CKD, cardiovascular disease (CVD) and osteodystrophy. Removal of indoxyl sulfate by AST-120 is a therapeutic strategy to delay the progression of not only CKD, but also CVD and osteodystrophy.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
