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NDT Advance Access originally published online on June 10, 2008
Nephrology Dialysis Transplantation 2008 23(8):2708-2709; doi:10.1093/ndt/gfn220
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Catheter locks, heparin and biofilm: what is this the risk?

E-mail: hndt512{at}bellsouth.net

Sir,

Dr Onder's work [1] once again demonstrates the efficacy of the value of antimicrobial catheter lock solutions (ALS) [2–6]; however, their work may add additional insight into the pathophysiology of biofilm. We have often speculated that the success of ALS over the traditional heparin lock might be possibly related to the fact that heparin itself may promote biofilm production [7] of most Staphylococcus through aiding quorum sensing [8]. If so, then the systemic heparin that flows through the catheter may also be a risk factor. We have recently evaluated risk factors for catheter-related sepsis (CRS) in 559 patients undergoing chronic maintenance haemodialysis and found that a prolonged duration of catheter use (P < 0.0001), a depressed serum albumin (P < 0.001), intravenous iron (P = 0.001) and a mid-treatment dose of heparin (P = 0.046) were the only variables that were associated with increased risk of sepsis (which was predominantly Staphylococcus, Table 1) [9]. While our data were not perfect, it may still lend some clinical evidence that the heparin itself is the risk factor for biofilm production and sepsis. The effect of heparin on biofilm, however, might vary for various strains of Staphylococcus. Onder's work now suggests that such may not be the case, since elimination of heparin did not improve the successful eradication of sepsis but actually tended to decrease it.


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Table 1 Organisms responsible for the catheter-related sepsis (N = 141) [7]

 
Does this suggest that heparin may not be a pathologic factor? Perhaps, yet unlike most series of CRS, Staphylococcus aureus was relatively uncommon in Onder's study and indeed only one case was assigned to the heparin arm. In contrast, both coagulase negative Staphylococcus and Enterobacter were four times as common infecting agents in the heparin arm as Staphylococcus aureus. Another investigator recently found that in vitro heparin caused detachment of Staphylococcus lugdunensis from catheter walls [10], which could theoretically either inhibit biofilm formation [11] or alternatively promote sepsis through systemic dispersal of biofilm [12]. The unusual distribution of bacterial pathogens in Dr Onder's work may have therefore either distorted his results, or alternatively may have given us valuable insight into the lack of an effect heparin on CRS.

Conflict of interest statement. All authors have no conflicts of interest.

Charles J. Diskin, Thomas J. Stokes, Linda Dansby, Lautrec Radcliff and Thomas B. Carter

Hypertention, Nephrology, Dialysis and Transplantation, Auburn University, Opelika, AL, USA

Notes

Editorial Note: Dr Onder et al. declined the opportunity to reply to this letter.

References

  1. Onder AM, Chandar J, Simon N, et al. Comparison of tissue plasminogen activator-antibiotic locks with heparin-antibiotic locks in children with catheter-related bacteraemia. Nephrol Dial Transplant (2008).
  2. Allon M. Prophylaxis against dialysis catheter-related bacteremia: a glimmer of hope. Am J Kidney Dis (2008) 51:165–168.[CrossRef][Web of Science][Medline]
  3. Allon M. Prophylactic effect of antibiotic lock solution on bacteremia related to use of uncuffed hemodialysis catheters. Nat Clin Pract Nephrol (2006) 2:418–419.[CrossRef][Web of Science][Medline]
  4. Poole CV, Carlton D, Bimbo L, et al. Treatment of catheter-related bacteraemia with an antibiotic lock protocol: effect of bacterial pathogen. Nephrol Dial Transplant (2004) 19:1237–1244.[Abstract/Free Full Text]
  5. Allon M. Prophylaxis against dialysis catheter-related bacteremia with a novel antimicrobial lock solution. Clin Infect Dis (2003) 36:1539–1544.[CrossRef][Web of Science][Medline]
  6. Krishnasami Z, Carlton D, Bimbo L, et al. Management of hemodialysis catheter-related bacteremia with an adjunctive antibiotic lock solution. Kidney Int (2002) 61:1136–1142.[CrossRef][Web of Science][Medline]
  7. Diskin CJ, Stokes TJ, Dansby LM, et al. Heparin and biofilm: is this the risk factor for catheter-related sepsis. Am J Kidney Dis (2008) 52:197–198.[CrossRef][Medline]
  8. Shanks RM, Donegan NP, Graber ML, et al. Heparin stimulates Staphylococcus aureus biofilm formation. Infect Immun (2005) 73:4596–4606.[Abstract/Free Full Text]
  9. Diskin CJ, Stokes TJ, Dansby LM, et al. Is systemic heparin a risk factor for catheter-related sepsis in dialysis patients? An evaluation of various biofilm and traditional risk factors. Nephron Clin Pract (2007) 107:c128–c132.[CrossRef][Web of Science][Medline]
  10. Frank KL, Patel R. Intravenously administered pharmaceuticals impact biofilm formation and detachment of Staphylococcus lugdunensis and other staphylococci. Diagn Microbiol Infect Dis (2007).
  11. Diskin CJ. Heparin, biofilm, and catheter-related sepsis. Diagn Microbiol Infect Dis (2008).
  12. Frank KL, Patel R. Response to Dr. Charles J. Diskin's submission ‘heparin, biofilm, and catheter-related sepsis’. Diagn Microbiol Infect Dis (2008).

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This Article
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