11
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Nodular lesions and mesangiolysis in diabetic nephropathy.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Diabetic nephropathy is a leading cause of end-stage renal failure all over the world. Advanced human diabetic nephropathy is characterized by the presence of specific lesions including nodular lesions, doughnut lesions, and exudative lesions. Thus far, animal models precisely mimicking advanced human diabetic nephropathy, especially nodular lesions, remain to be fully established. Animal models with spontaneous diabetic kidney diseases or with inducible kidney lesions may be useful for investigating the pathogenesis of diabetic nephropathy. Based on pathological features, we previously reported that diabetic glomerular nodular-like lesions were formed during the reconstruction process of mesangiolysis. Recently, we established nodular-like lesions resembling those seen in advanced human diabetic nephropathy through vascular endothelial injury and mesangiolysis by administration of monocrotaline. Here, in this review, we discuss diabetic nodular lesions and its animal models resembling human diabetic kidney lesions, with our hypothesis that endothelial cell injury and mesangiolysis might be required for nodular lesions.

          Related collections

          Author and article information

          Journal
          Clin. Exp. Nephrol.
          Clinical and experimental nephrology
          Springer Nature America, Inc
          1437-7799
          1342-1751
          Feb 2013
          : 17
          : 1
          Affiliations
          [1 ] Division of Nephrology, Kanazawa University Hospital, 13-1 Takara-machi, Kanazawa 920-8641, Japan. twada@m-kanazawa.jp
          Article
          10.1007/s10157-012-0711-6
          23100177
          4c14164e-bbec-4e80-81f4-6d28b36a17a0
          History

          Comments

          Comment on this article