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NDT Advance Access originally published online on April 23, 2007
Nephrology Dialysis Transplantation 2007 22(10):3088-3089; doi:10.1093/ndt/gfl829
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org



Significance of endotoxaemia in chronic kidney disease

Email: tetsu{at}jg8.so-net.ne.jp

Sir,

I read with great interest the recent article of Gon{varepsilon}alves and colleagues [1] on the association between mild endotoxaemia and fluid overload or inflammatory markers in patients with chronic kidney disease (CKD). They concluded that mild endotoxaemia was linked to fluid overload although there was no association between circulating endotoxin concentrations and systemic inflammation.

Recently, there is an increasing evidence to suggest that a leaky bowel wall may lead to translocation of bacteria and/or endotoxin, which may be an important stimulus for inflammatory cytokine activation, leading to the progression of chronic heart failure [2]. Similarly, endotoxin translocation could be associated with the deterioration of renal function in patients with CKD. This hypothesis provides a plausible mechanism for the downward systemic course that commonly occurs in patients with end-stage renal disease, in which bowel wall oedema, mesenteric hypoperfusion, or both, are likely.

The presence of endotoxin in minute amounts in blood was reported in 80% of healthy individuals [3]. Mild to modest endotoxaemia has been observed after elective abdominal surgery [4], strenuous exercise [5] and in patients with liver cirrhosis [6]. Usually, the degree of endotoxaemia is not related to the circulating cytokine or acute-phase protein concentrations. As written in the discussion of the article, endotoxin concentrations (0.16–1.4 ng/l) in patients with CKD are too low to produce systemic inflammatory response. Moreover, the value of 1.4 pg/ml (1.4 ng/l), which is the minimum detection limit of the LAL assay used in the study, exceeds almost all of the data.

Conflict of interest statement. None declared.

Tetsuji Fujita

Department of Surgery
Jikei University School of Medicine
Tokyo, Japan

References

  1. 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]
  2. 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]
  3. 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]
  4. 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]
  5. 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]
  6. Endotoxin levels measured by a chromogenic assay in portal, hepatic and peripheral venous blood in patients with cirrhosis. Hepatology (1988) 8:232–236.[Web of Science][Medline]

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This Article
Right arrow Extract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
22/10/3088    most recent
gfl829v1
Right arrow Alert me when this article is cited
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Right arrow Articles by Fujita, T.
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