title: [The uremic toxin, indoxyl sulfate, signifies cardio-renal risk and intestinal-renal relationship].
abstract: Uremic syndrome and condition is primarily a result of kidney failure in which uremic toxins are accumulated. More and more attention is paid to possibilities for removal of uremic toxins, which not only means dialysis, but also takes into account special dietary considerations and treatments, which aim to absorb the toxins or reduce their production. These uremic toxins, which also increase the cardiovascular risks, play a major part in morbidity and mortality of patients suffering from chronic renal failure and those receiving renal replacement therapy. One of them is a member of the indol group, the indoxyl sulfate. This toxin is difficult to remove with dialysis and is an endogenous protein-bound uremic toxin. Today we know that indoxyl sulfate is a vascular-nephrotoxic agent, which is able to enhance progression of cardiovascular and renal diseases. It is of particular importance that because of its redox potency, this toxin causes oxidative stress and antioxidant effects at the same time and, on top of that, it is formed in the intestinal system. Its serum concentration depends on the nutrition and the tubular function and, therefore, it can also signal the progression of chronic renal failure independently of glomerular filtration rate. Successful removal of indoxyl sulfate reduces the morbidity and mortality and improves survival. Therefore, it could be a possible target or area to facilitate the reduction of uremia in chronic renal failure. The use of probiotics and prebiotics with oral adsorbents may prove to be a promising opportunity to reduce indoxyl sulfate accumulation.
authors: Fővárosi Önkormányzat Szent Imre Kórház, Belgyógyászati Szakmák Mátrix Intézete, Nephrologia-Hypertonia Profil és B. Braun Avitum, Hungary. ikiss@enternet.hu
authors: István
authors: I
authors: Kiss
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D018450:Disease Progression; D006801:Humans; D007200:Indican / Q000096:biosynthesis / Q000097:blood / Q000737:chemistry / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000503:physiopathology*; D007668:Kidney / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D012307:Risk Factors; D014511:Uremia / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D007200:Indican