[Clinical and metabolic consequences of uremic toxicity]

Retention of many substances takes place in the pathogenesis of uremic toxicity. There are almost 100 different molecules described and defined as uremic toxins. These substances are divided into three groups according to EUTOX group calssification. Small water soluble molecules with a molecular weight less than 500 D are included into the first group. Derivate of guanidines, purines, pyrimidines and methyloamines appeared in this group. There is also an unclassified subgroup with urea as a "classical" toxin which the real role in the uraemic syndrome is still discussed. Main symptoms caused by these molecules are digestive disturbances, neurological changes, hypertension etc. We can eliminate almost all of these toxins with standard methods used during dialysotherapy. Substances with a different molecular weight but connected with proteins determine the second group. AGE-s, phenol derivates, leptin and poliamines beside others create this group. There are many studies that have proved that these toxins cause hypertension, arteriosclerosis and shortened life time of hemodialysed patients. However, melatonin toxicity is not fully proved. Different types of renal replacement therapy are not valid to purify blood from protein-bound substances. Middle molecules are included into the third group, with a molecular weight higher than 500 D. There are cytokines, neuro-transmitters e.g. beta-endorphin, metencephalin and many others accounted into this group. One of them is the parathormon, well known and considered as "universal" toxin for several years. Middle molecules are causing very different effects. They are responsible for: anemia, arteriosclerosis, chronic inflammation and generally increase dialysed patient mortality. Toxic action of several molecules described below is still not proved; however there are some ongoing studies aimed to find pathophysiological links between old and new described uremic toxins.