NDT Advance Access originally published online on April 23, 2007
Nephrology Dialysis Transplantation 2007 22(10):3089; doi:10.1093/ndt/gfm200
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Reply
Email: r.pecoits{at}pucpr.brSir,
It was interesting to read the letter to the editor commenting on our manuscript recently published in Nephrology, Dialysis and Transplantation [1]. The authors of the letter kindly recognize the importance of our contribution to the understanding of potential causes of the inflammatory response observed in chronic kidney disease (CKD) patients. They also comment on our findings of the lack of association between endotoxaemia and the levels of inflammation markers, which we will briefly discuss.
Initially, it must be emphasized that our study is a clinical observational investigation that was not controlled for many factors. Therefore, as clearly stated in the discussion of our article, the aim of the study was the establishment of associations, and could not safely enter the field of mechanisms.
In the last part of the letter, the authors correctly observed that most of the values of plasma endotoxin presented in our study appear to be below the detection limit of the method utilized. This was due to an error in the conversion of the units, which will be acknowledged in errata. In the results section, values should have been presented in ng/ml instead of ng/l as presented in the article. The corrected results indicate that most patients in our study present levels compatible to what is considered mild to moderate endotoxaemia. Finally, with respect to our statement, that the lack of correlation between levels of endotoxin and inflammation markers observed in our study could be explained by insufficient amounts of circulating endotoxin, we believe that it is impossible at the moment to present a definitive answer. Although most published data in other populations have not shown a significant correlation between inflammation markers and endotoxin levels [2,3], data on healthy individuals [4] show a significant correlation between endotoxaemia and C-reactive protein after ultra-endurance exercise, in levels (5-15pg/ml) much lower than observed in our CKD patients. Furthermore, raised concentrations (in similar levels when compared with our findings) of endotoxin and cytokines are found in patients with oedematous chronic heart failure, which are normalized after diuretic treatment [5]. In the search for causes of inflammation activation in the progression of CKD, further studies with adequate design will need to address these issues.
Conflict of interest statement. None declared.
Center for Health
and Biological Sciences
Pontificia Universidade Catolica do
Parana Curitiba
Brazil
References
- Goncalves S, Pecoits-Filho R, Perreto S, et al. Association between renal function, volume status and endotoxaemia in chronic kidney disease patients. Nephrol Dial Transplant (2006) 21:2788–2794.
[Abstract/Free Full Text] - Goto T, Eden S, Nordenstam G, Sundh V, Svanborg-Eden C, Mattsby-Baltzer I. Endotoxin levels in sera of elderly individuals. Clin Diagn Lab Immunol (1994) 1:684–688.[Medline]
- Fujita T, Imai T, Anazawa S. Influence of modest endotoxemia on postoperative antithrombin deficiency and circulating secretory immunoglobulin A levels. Ann Surg (2003) 238:258–263.[Web of Science][Medline]
- Jeukendrup AE, Vet-Joop K, Sturk A, et al. Relationship between gastro-intestinal complaints and endotoxaemia, cytokine release and the acute-phase reaction during and after a long-distance triathlon in highly trained men. Clin Sci (2000) 98:47–55.[CrossRef][Web of Science][Medline]
- Niebauer J, Volk HD, Kemp M, et al. Endotoxin and immune activation in chronic heart failure: a prospective cohort study. Lancet (1999) 353:1838–1842.[CrossRef][Web of Science][Medline]
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