Background Uric Acid (UA) is filtered at the glomeruli and absorbed at the tubule, so only 7-12% of the filtered UA is finally excreted. It has been shown that Serum Uric Acid (SUA) can lower during an acute gout flare. These changes in SUA result from an increase in renal fractional excretion of UA (FE_UA) and correlate to the intensity of inflammation. SUA also drops during other acute inflammatory events such as surgical critically ill patients, though pathogenesis remains here unclear.
Objectives Our aim is to determine whether during overwhelming septic systemic inflammatory response syndrome (SIRS) changes in SUA related to alterations in UA renal handling do occur and to gauge its possible significance.
Methods We prospectively recruited patients meeting established criteria for severe sepsis or septic shock who were admitted in our Intensive Care Unit since May 2010. APACHE II score was used to evaluate clinical severity during the first 24 hours following ICU admission and SUA and FE_UA were measured in each patient. None of them was on UA-lowering medication. The study is ongoing.
Results 17 consecutive patients (9 men:8 women) with diagnosis of severe sepsis (n=11) and septic shock (n=6) of different origins were included. Age: 73 years (IQR 54-78). Median APACHE II: 17 (IQR 13-24). FE_UA was above 12% in 15 patients (82%). FE_UA median was 22% (IQR 14-40) -normal 7-12%>. SUA median was 2.9 mg/dl (IQR 1.3-5.7). Seven patients (41.2%) had hypouricemia (SUA <2.5 mg/dl). There was an inverse correlation between SUA and FE_UA (p=-0.569 [p<0.05]). Presence of shock associated with lower SUA and higher FE_UA (SUA: p=-0.503 [p<0.05]; FE_UA: p=0.779 [p<0.01]). Noteworthy, FE_UA exhibited a significant positive correlation with APACHE II score (p=0.539 [p<0.05]).
Conclusions A raised excretion of UA (measured as FE_UA) resulting in low SUA levels was noted in patients with septic SIRS; higher increases in FE_UA correlated with higher APACHE II scores. This strongly suggests that the drop of SUA might be a usual consequence related to acute inflammation that appears largely explained by a higher renal clearance of urate. The underlying urate renal handling mechanisms still need clarification. Whether the relation found with APACHE II may have clinical or prognostic implications requires further studies.
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Disclosure of Interest None Declared