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NDT Advance Access originally published online on October 13, 2006
Nephrology Dialysis Transplantation 2007 22(2):592-596; doi:10.1093/ndt/gfl584
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

P-cresylsulphate, the main in vivo metabolite of p-cresol, activates leucocyte free radical production

Eva Schepers1, Natalie Meert1, Griet Glorieux1, Jan Goeman2, Johan Van der Eycken2 and Raymond Vanholder1

1Renal Division, Department of Internal Medicine, University Hospital Gent and 2Laboratory for Organic and Bio-organic Synthesis, Department of Organic Chemistry, Gent University, Gent, Belgium

Correspondence and offprint requests to: R. Vanholder, Renal Division, Department of Internal Medicine, University Hospital, De Pintelaan 185, 9000 Gent, Belgium. Email: Raymond.Vanholder{at}UGent.be



  Abstract

Background. Chronic renal insufficiency is associated with the retention of solutes normally excreted by healthy kidneys. P-cresol, a prototype protein-bound uraemic retention solute, has been shown to exert toxic effects in vitro. Recently, however, it has been demonstrated that p-cresol in the human body is conjugated, with p-cresylsulphate as the main metabolite.

Methods. The present study evaluates the effect of p-cresylsulphate on the respiratory burst activity of leucocytes.

Results. P-cresylsulphate significantly increased the percentage of leucocytes displaying oxidative burst activity at baseline. Oxidative burst activity of stimulated leucocytes was however not affected. In contrast, p-cresol had no effect on the leucocytes at baseline, but inhibited leucocytes burst activity after stimulation.

Conclusion. The present study demonstrates, for the first time, that p-cresylsulphate, the main in vivo metabolite of p-cresol, has a pro-inflammatory effect on unstimulated leucocytes. This effect could contribute to the propensity to vascular disease in the uraemic population.

Keywords: immune response; leucocytes; oxidative burst activity; uraemic toxins; vascular disease


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