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found in interstitial fl uid, plasma, lymph and synovial fl uid. Few studies have looked at SOD activity and its expression in CKD patients; the present study by Akiyama et al. [8] published in this issue of Nephron Clinical Practice is one of them. The authors found a signifi cant increase in SOD activity in leucocytes in CKD patients, but this increase affects only Cu/Zn-SOD. Moreover, Cu/ZnSOD mRNA expression in leucocytes was also signifi cantly higher as compared to controls. This latter result is in line with an earlier study [9] , in which an increase in SOD expression in white blood cells in CKD patients was also found. However, this increase in SOD activity is in contrast to the results of several studies, in which a decrease in erythrocyte SOD activity in CKD patients was observed [5, 10, 11] . Furthermore, we must be careful when comparing these different studies, since different sources of cells were used. Knowing that erythrocytes in CKD patients could have a shorter life span because of anemia, it is possible that this shorter life span could explain the difference in SOD levels between these studies. This discrepancy raises the question as to the ideal blood element in which to evaluate SOD activity in CKD patients. The role of SOD and its different isoforms in the antioxidant defence mechanism in CKD patients is currently unclear. In light of the importance of myeloperoxydase Chronic kidney disease (CKD) is commonly reported to be associated with oxidative stress but there is still controversy on the mechanism. Numerous sources of radical oxygen species (ROS) have been identifi ed in CKD patients, especially in hemodialysis (HD) patients. Macrophage activation, which produces ROS, is due in these patients to: accumulation of uremic toxins; dialysis membrane bio-incompatibility; infl ux of endotoxins from the dialysate, and immunologic and metabolic disorders such as diabetes and dyslipidemia [1] . Phagocyte myeloperoxidase-mediated events have also been associated with the production of oxidized low-density lipoprotein [2] ; advanced oxidation protein products and advanced glycation end products, which are considered potent mediators of infl ammation [3] . Moreover, treatment of anemia with high levels of iron may induce oxidative stress [4] . The massive generation of ROS is all the more damaging given that CKD patients have a weaker antioxidant system due to a diet low in antioxidant vitamins and oligoelements [5] and due to loss of antioxidants during HD sessions [6] . The superoxide dismutase (SOD) is the front line of defence against superoxide anions (O 2 – ) and detoxifi es O 2 – into hydrogen peroxide (H 2 O 2 ). SOD is a metalloenzyme existing in three different isoforms [7] : the cytoplasmic copper-zinc SOD (Cu/Zn-SOD); the mitochondrial manganese SOD (Mn-SOD) and the extracellular SOD Published online: April 11, 2005

Dysregulation of Superoxide Dismutase in Chronic Kidney Disease