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Gut 2009;58:443-449 doi:10.1136/gut.2008.154120
  • Hepatology

The systemic inflammatory response syndrome is predictive of renal dysfunction in patients with non-paracetamol-induced acute liver failure

  1. J A Leithead,
  2. J W Ferguson,
  3. C M Bates,
  4. J S Davidson,
  5. A Lee,
  6. A J Bathgate,
  7. P C Hayes,
  8. K J Simpson
  1. Scottish Liver Transplant Unit, Royal Infirmary of Edinburgh and University of Edinburgh, Edinburgh, UK
  1. Dr J A Leithead, Scottish Liver Transplant Unit, Royal Infirmary of Edinburgh, 51, Little France Crescent, Edinburgh EH16 4SA, UK,; jleithea{at}staffmail.ed.ac.uk
  • Revised 22 September 2008
  • Accepted 28 October 2008
  • Published Online First 10 November 2008

Abstract

Background: Although renal dysfunction is a common complication of acute liver failure (ALF) with significant prognostic implications, the pathophysiological mechanisms remain unclear. The current hypothesis suggests that the renal dysfunction may mirror the hepatorenal syndrome of cirrhosis. However, ALF has distinct clinical characteristics and the circulatory derangement may be more comparable with sepsis.

Objectives: To examine the relationship between the systemic inflammatory response syndrome (SIRS) and renal dysfunction in ALF, and to identify additional risk factors for renal dysfunction.

Methods: A single-centre retrospective study of 308 patients with ALF was carried out. Renal dysfunction was defined according to the RIFLE criteria for acute kidney injury.

Results: 67% of patients developed renal dysfunction. On univariate analysis, renal dysfunction patients were more likely to be hypothermic (p = 0.010), had a faster heart rate (p<0.001), a higher white cell count (p = 0.001) and a lower PaCO2 (p = 0.033). 78% of renal dysfunction patients and 53% of non-renal dysfunction patients had SIRS (p<0.001). On multivariate analysis, the risk factors for renal dysfunction were age (p = 0.024), fulfilled Kings College Hospital prognostic criteria (p<0.001), hypotension (p<0.001), paracetamol-induced ALF (p<0.001), infection (p = 0.077) and SIRS (p = 0.017). SIRS remained an independent predictor of renal dysfunction in the subgroup of patients with non-paracetamol-induced ALF (n = 91, p = 0.001). In contrast, in patients with paracetamol-induced ALF (n = 217), no relationship between SIRS and renal dysfunction was demonstrated (p = 0.373).

Conclusion: SIRS is strongly associated with the development of renal dysfunction in patients with non-paracetamol-induced ALF. It is proposed that the systemic inflammatory cascade plays a key role in its pathogenesis.

Footnotes

  • Competing interests: None.

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