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NDT Advance Access originally published online on October 3, 2007
Nephrology Dialysis Transplantation 2008 23(1):421-422; doi:10.1093/ndt/gfm629
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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



Sodium citrate anticoagulation during sustained low efficiency dialysis (SLED) in patients with acute renal failure and severely impaired liver function

Email: christian.morath{at}med.uni-heidelberg.de

Sir,

Due to severe side effects, sodium citrate anticoagulation has been avoided in patients with severely impaired liver function undergoing renal replacement therapy [1]. Based on a previously published protocol, seven patients with acute renal failure (diagnosed according to accepted guidelines) and severely impaired liver function (mean Child–Pugh score: 10.5 ± 0.5) received a total of 10 sustained low efficiency dialysis (SLED) treatments using the Genius dialysis system [2–4]. For this study, a high-flux membrane (FX 50, Fresenius Medical Care, Bad Homburg, Germany) was used. The dialysate contained 1.0 mmol/L calcium, 30 mmol/L bicarbonate and 135 mmol/L (n = 9) or 138 mmol/L (n = 1) sodium. Three percent sodium citrate (110.9 mmol/L; Fresenius Medical Care, Bad Homburg, Germany) was infused pre-filter at a rate to maintain the post-filter ionized calcium levels between 0.6 and 0.7 mmol/L. There was no routine calcium supplementation at the venous line (supplemental Figure 1). Mean patient age was 61.7 ± 4.8 years. APACHE II and SOFA score were 34.6 ± 3.4 and 16.4 ± 0.8, respectively. Laboratory values are given in Table 1. All patients were on daily dialysis before initiation of SLED therapy with sodium citrate anticoagulation. The rationale for sodium citrate anticoagulation was repeated filter clotting (filter lifetime <2 h) under heparin-free or low-dose heparin therapy. Mean dialysis time with sodium citrate anticoagulation was 17.3 ± 4.1 h. There was a mean of 0.043 ± 0.017 clotting events per h, translating to a mean (theoretical) filter lifetime of 23.3 h. No major bleeding episodes related to the dialysis therapy were observed. Total calcium, ionized calcium, calcium gap (total calcium – ionized calcium), electrolytes and base excess (as well as other parameters of acid–base balance) were maintained at stable levels during therapy and thereafter (Table 1 and supplemental Figure 2). This was also applicable in repeated SLED treatments using sodium citrate anticoagulation in the same patient. There were no significant hypotensive episodes during SLED therapy and norepinephrine dosage was significantly reduced during therapy (P < 0.04; Table 1). Our observation is in contrast with previous publications, where sodium citrate anticoagulation in patients with impaired liver function led to severe disturbances of electrolytes, acid–base haemostasis or even death [1]. The main difference between our protocol and conventional protocols is the lower sodium citrate infusion rate with higher targeted post-filter ionized calcium levels and the absence of routine calcium supplementation at the venous line. The risk of accumulating calcium-citrate complexes is further reduced by elimination of citrate complexes by high-flux dialysis [2,5]. This protocol offers the unique opportunity for sodium citrate anticoagulation in patients with even pronounced impairment of liver function. However, in the absence of serum citrate measurements and clearance determinations, accumulation of citrate complexes with longer duration of treatment or repeated treatments cannot be entirely excluded.


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Table 1. Laboratory values and treatment parameters for 10 SLED treatments

 

Christian Morath1, Nexhat Miftari1, Ralf Dikow1, Christian Hainer2, Martin Zeier1, Stanislao Morgera3, Markus A. Weigand2 and Vedat Schwenger1

1Department of Nephrology
University of Heidelberg
Heidelberg, Germany 2Clinic of Anesthesiology
University of Heidelberg
Heidelberg, Germany 3Department of Nephrology
Charité University of Berlin
Berlin, Germany

Acknowledgements

The authors would like to thank the dialysis staff (headed by Andreas Neumann) and intensive care unit staff (headed by Angelika Brobeil) at the Department of General Surgery and the Clinic of Anesthesiology at the University of Heidelberg for their support in the SLED dialysis programme.

Conflict of interest statement. None declared.

Supplementary material. Supplementary material is available at www.oxfordjournals.org.

Notes

See http://www.oxfordjournals.org/our_journals/ndtplus/

References

  1. Nowak MA, Campbell TE. Profound hypercalcemia in continuous veno-venous hemofiltration dialysis with trisodium citrate anticoagulation and hepatic failure. Clin Chem (1997) 43:412–413.[Free Full Text]
  2. Morgera S, Scholle C, Melzer C, et al. A simple, safe and effective citrate anticoagulation protocol for the Genius dialysis system in acute renal failure. Nephron Clin Pract (2004) 98:c35–c40.[CrossRef][Web of Science][Medline]
  3. Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet (2005) 365:417–430.[Web of Science][Medline]
  4. Morath C, Miftari N, Dikow R, et al. Renal replacement therapy in the intensive care unit. Anaesthesist (2006) 55:901–913. quiz 914.[CrossRef][Web of Science][Medline]
  5. Kramer L, Bauer E, Joukhadar C, et al. Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients. Crit Care Med (2003) 31:2450–2455.[CrossRef][Web of Science][Medline]

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