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<article article-type="letter" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML">
  <front>
    <journal-meta>
      <journal-id journal-id-type="pmc">JRMS</journal-id>
      <journal-id journal-id-type="pubmed">J Res Med Sci</journal-id>
      <journal-id journal-id-type="publisher-id">Journal of Research in Medical Sciences</journal-id>
      <journal-title>Journal of Research in Medical Sciences</journal-title>
      <issn pub-type="ppub">1735-1995</issn>
      <issn pub-type="epub">1735-7136</issn>
      <publisher>
        <publisher-name>Medknow Publications Pvt Ltd</publisher-name>
        <publisher-loc>India</publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">JRMS-18-628</article-id>
      <article-categories>
        <subj-group subj-group-type="headings">
          <subject>Letter To Editor</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Ameliorative effects of metformin on renal histologic and biochemical alterations of gentamicin-induced renal toxicity in Wistar rats</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Nasri</surname>
            <given-names>Hamid</given-names>
          </name>
          <xref ref-type="aff" rid="aff1" />
          <xref ref-type="corresp" rid="cor1" />
        </contrib>
      </contrib-group>
      <aff id="aff1">Department of Nephrology, Division of Nephropathology, Isfahan University of Medical Sciences, Isfahan, Iran</aff>
      <author-notes>
        <corresp id="cor1">
        <bold>Address for correspondence:</bold>Hamid Nasri, Department of Nephrology, Division of Nephropathology, Isfahan University of Medical Sciences, Isfahan, Iran 
        <email xlink:href="hamidnasri@med.mui.ac.ir">hamidnasri@med.mui.ac.ir</email></corresp>
      </author-notes>
      <pub-date pub-type="ppub">
        <season>July</season>
        <year>2013</year>
      </pub-date>
      <volume>18</volume>
      <issue>7</issue>
      <fpage>628</fpage>
      <lpage>628</lpage>
      <permissions>
        <copyright-statement>Copyright: &#x000a9; Journal of Research in Medical Sciences</copyright-statement>
        <copyright-year>2013</copyright-year>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0">
          <p>This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
        </license>
      </permissions>
    </article-meta>
  </front>
  <body>
    <sec>
      <title />
      <p>Sir,</p>
      <p>Recently, we published an article in J Res Med Sci, entitled "Ameliorative effects of metformin on renal histologic and biochemical alterations of gentamicin-induced renal toxicity in Wistar rats." 
      <sup>
        <xref ref-type="bibr" rid="ref1">1</xref>
      </sup>In this article, it is concluded that metformin (MF) may prevent or ameliorate GM-induced acute renal failure, and therefore, it might be beneficial in patients under treatment with this medicine. 
      <sup>
        <xref ref-type="bibr" rid="ref1">1</xref>
      </sup>In this letter, we would like to point out a few points about the mentioned conclusion. In an agreement with our findings, Taheri et al. recently conducted a study on the effects of MF on renal function and structure after unilateral ischemia-reperfusion in rat. They found that MF provided some renal protection against ischemia and reperfusion (I/R) induced injury to the rats kidney. They concluded that MF with activation of adenosine monophosphate-activated protein kinase (AMPK) and endothelial nitric oxide synthase have tissue protective effects. 
      <sup>
        <xref ref-type="bibr" rid="ref2">2</xref>
      </sup>More recently, Kim et al. performed a study using MF (350 mg/kg/day) for spontaneously diabetic Torii (SDT) rats for 17 weeks. They examined blood glucose, glycated hemoglobin and albuminuria, kidney histopathology, renal 8-hydroxydeoxyguanosine levels, and also apoptosis. They found that treatment of SDT rats with MF restored podocyte loss. They suggested that diabetes-induced podocyte loss in diabetic nephropathy could be suppressed by MF, through the repression of oxidative injury. 
      <sup>
        <xref ref-type="bibr" rid="ref3">3</xref>
      </sup></p>
      <p>Diabetic nephropathy is one of the most important complication of diabetes mellitus 
      <sup>
        <xref ref-type="bibr" rid="ref4">4</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref5">5</xref>
      </sup>and MF has been widely used for treatment of type 2 diabetes. 
      <sup>
        <xref ref-type="bibr" rid="ref3">3</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref4">4</xref>
      </sup>Thus according to our results and those published by Taheri et al., MF protects against tubular injury by restoring the biochemical alterations and modulation of oxidative stress on the tubules. 
      <sup>
        <xref ref-type="bibr" rid="ref1">1</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref2">2</xref>
      </sup>Moreover, according to the study by Kim et al., MF protects podocytes in diabetic nephropathy, 
      <sup>
        <xref ref-type="bibr" rid="ref3">3</xref>
      </sup>while in diabetic nephropathy, there is also tubular cell injury due to glocosuria. 
      <sup>
        <xref ref-type="bibr" rid="ref3">3</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref4">4</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref5">5</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref6">6</xref>
      </sup>,
      <sup>
        <xref ref-type="bibr" rid="ref7">7</xref>
      </sup>These findings can more potentiate the clinical use of MF in the prevention of diabetic nephropathy. In this regard, to understand the MF-nephroprotective properties better, more experimental rat model or clinical studies are suggested.</p>
    </sec>
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