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<art>
   <ui>cc7416</ui>
   <ji>CCJ</ji>
   <fm>
      <dochead>Poster presentation</dochead>
      <bibl>
         <title>
            <p>Urinary glutathione S-transferase as an early marker for acute kidney injury in patients admitted to intensive care with sepsis</p>
         </title>
         <aug>
            <au id="A1">
               <snm>Walshe</snm>
               <fnm>C</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A2">
               <snm>Odejayi</snm>
               <fnm>F</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A3">
               <snm>Ng</snm>
               <fnm>S</fnm>
               <insr iid="I1"/>
            </au>
            <au id="A4">
               <snm>Marsh</snm>
               <fnm>B</fnm>
               <insr iid="I1"/>
            </au>
         </aug>
         <insg>
            <ins id="I1">
               <p>Mater Misericordiae University Hospital, Dublin, Ireland</p>
            </ins>
         </insg>
         <source>Critical Care</source>
         <supplement>
            <title>
               <p>29th International Symposium on Intensive Care and Emergency Medicine</p>
            </title>
            <url>http://ccforum.com/supplements/notes/ccv13s1-info.pdf</url>
         </supplement>
         <conference>
            <title>
               <p>29th International Symposium on Intensive Care and Emergency Medicine</p>
            </title>
            <location>Brussels, Belgium</location>
            <date-range>24&#8211;27 March 2009</date-range>
            <url>http://www.intensive.org/</url>
         </conference>
         <issn>1364-8535</issn>
         <pubdate>2009</pubdate>
         <volume>13</volume>
         <issue>Suppl 1</issue>
         <fpage>P252</fpage>
         <url>http://ccforum.com/content/13/S1/P252</url>
         <xrefbib>
            <pubid idtype="doi">10.1186/cc7416</pubid>
         </xrefbib>
      </bibl>
      <history>
         <pub>
            <date>
               <day>13</day>
               <month>3</month>
               <year>2009</year>
            </date>
         </pub>
      </history>
      <cpyrt>
         <year>2009</year>
         <collab>Walshe et al; licensee BioMed Central Ltd.</collab>
      </cpyrt>
   </fm>
   <bdy>
      <sec>
         <st>
            <p>Introduction</p>
         </st>
         <p>Acute kidney injury (AKI) is common in patients admitted to intensive care. Diagnosis of AKI relies on serum creatinine and urine flow. These have disadvantages of low specificity and sensitivity and a slow rate of change. Renal damage results in release of tubular enzymes into the urine. Measurement of urinary alpha glutathione S-transferase (&#945;GST) and pi glutathione S-transferase (&#960;GST) may indicate AKI more acutely and accurately than current methods of diagnosis.</p>
      </sec>
      <sec>
         <st>
            <p>Methods</p>
         </st>
         <p>Urine was collected from patients with a sepsis diagnosis 4 hourly over 48 hours. Urine was frozen, and urinary &#960;GST and &#945;GST measured. Fluid and vasopressor management was recorded, but managed independently. Serum creatinine was measured at 0, 24 and 48 hours. AKI was diagnosed using AKI Network criteria <abbrgrp><abbr bid="B1">1</abbr></abbrgrp>.</p>
      </sec>
      <sec>
         <st>
            <p>Results</p>
         </st>
         <p>We present the first 35 patients recruited, 20 were male, 15 female. Median patient age was 53 years. Median APACHE II score was 13. Median ICU length of stay was 9 days. ICU mortality was 14%, hospital mortality 23%. AKI was diagnosed in 26% of patients. Statistical significance was tested by Wilcoxon signed-rank test. Although the median &#960;GST at 0 hours was elevated (11.8 &#956;g/l (non-AKI) versus 22 &#956;g/l (AKI)) this was not statistically significant between the two groups, <it>P </it>= 0.985. &#960;GST did not demonstrate an increased urinary level in AKI versus non-AKI (median values 0.89 &#956;g/l vs. 3.4 &#956;g/l at 0 hours). See Figure <figr fid="F1">1</figr>.</p>
         <fig id="F1">
            <title>
               <p>Figure 1</p>
            </title>
            <caption>
               <p/>
            </caption>
            <text>
               <p/>
            </text>
            <graphic file="cc7416-1"/>
         </fig>
      </sec>
      <sec>
         <st>
            <p>Conclusion</p>
         </st>
         <p>A trend towards early expression of &#960;GST was identifiable in this study. This may indicate early detection of AKI, which may help guide therapeutic interventions. &#960;GST does not seem to be released as a biomarker using this sepsis model, suggesting a more specific distal tubular injury. Further work is required to determine levels of &#960;GST in nonstressed kidneys.</p>
      </sec>
   </bdy>
   <bm>
      <refgrp>
         <bibl id="B1">
            <title>
               <p>Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury</p>
            </title>
            <aug>
               <au>
                  <snm>Mehta</snm>
                  <fnm>RL</fnm>
               </au>
               <etal/>
            </aug>
            <source>Crit Care</source>
            <pubdate>2007</pubdate>
            <volume>11</volume>
            <fpage>R31</fpage>
            <xrefbib>
               <pubidlist>
                  <pubid idtype="pmcid">2206446</pubid>
                  <pubid idtype="pmpid" link="fulltext">17331245</pubid>
                  <pubid idtype="doi">10.1186/cc5713</pubid>
               </pubidlist>
            </xrefbib>
         </bibl>
      </refgrp>
   </bm>
</art>
