Abstract
This study showed that indoxyl sulfate, an uremic toxin present in the serum of patients with chronic kidney disease, increases oxidative stress and apoptosis in human neutrophils and reduces the production of monocyte chemoattractant protein-1 (MCP-1) by peripheral blood mononuclear cell (PBMC). It is possible that these effects caused by this toxin contribute to vascular injury of the endothelium and decreased response to infectious insults, respectively.
Highlights
Uremic toxins are solutes that accumulate in the plasma of patients with loss of renal function [1,2,3,4]
Apoptosis detected by annexin V (47% ± 11% versus 36% ± 11%; P = 0.0001) and CD95 expression (110±29 versus 48±21 mean fluorescence intensity (MFI); P = 0.0001) were higher in neutrophils incubated in the presence of indoxyl sulfate (IS) (Figures 1 and 2, resp.)
We observed increased apoptosis in neutrophils incubated with IS compared to control
Summary
Uremic toxins are solutes that accumulate in the plasma of patients with loss of renal function [1,2,3,4]. Uremic toxins have been considered one of the main factors that contribute to the state of inflammation [7,8,9] and have been associated with immune dysfunction in patients with chronic kidney disease (CKD) [10,11,12,13,14,15,16,17] They have been associated with cardiovascular disease (CVD), because of their effects on different cells types leading to the generation of reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), hydroxyl radical (OH−), and superoxide anion (O2−) [18, 19] that contribute to oxidization of lipids, protein, and DNA damage. MCP-1 is produced by a variety of cell types, either constitutively or after induction by toxins, oxidative stress, cytokines, or growth factors
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