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The systemic inflammatory response syndrome is predictive of renal dysfunction in patients with non-paracetamol-induced acute liver failure
  1. Joanna A Leithead (jleithea{at}staffmail.ed.ac.uk)
  1. Royal Infirmary of Edinburgh, United Kingdom
    1. James W Ferguson (j.w.ferguson{at}ed.ac.uk)
    1. Royal Infirmary of Edinburgh, United Kingdom
      1. Caroline M Bates (caroline.bates{at}luht.scot.nhs.uk)
      1. Royal Infirmary of Edinburgh, United Kingdom
        1. Janice S Davidson (janice.davidson{at}luht.scot.nhs.uk)
        1. Royal Infirmary of Edinburgh, United Kingdom
          1. Alistair Lee (alistair.lee{at}luht.scot.nhs.uk)
          1. Royal Infirmary of Edinburgh, United Kingdom
            1. Andrew J Bathgate (andy.bathgate{at}luht.scot.nhs.uk)
            1. Royal Infirmary of Edinburgh, United Kingdom
              1. Peter C Hayes (p.hayes{at}ed.ac.uk)
              1. Royal Infirmary of Edinburgh, United Kingdom
                1. Kenneth J Simpson (k.simpson{at}ed.ac.uk)
                1. Royal Infirmary of Edinburgh, United Kingdom

                  Abstract

                  Background: Although renal dysfunction is a common complication of acute liver failure (ALF) with significant prognostic implications the pathophysiological mechanisms remain unclear. 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: Single-centre retrospective study of 308 patients with ALF. 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. We propose that the systemic inflammatory cascade plays a key role in its pathogenesis.

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