Tubular atrophy in the pathogenesis of chronic kidney disease progression.

The longstanding focus in chronic kidney disease (CKD) research has been on the glomerulus, which is sensible because this is where glomerular filtration occurs, and a large proportion of progressive CKD is associated with significant glomerular pathology. However, it has been known for decades that...

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Publicado en:Pediatric Nephrology Vol. 31; no. 5; pp. 693 - 707
Autor principal: Schelling, Jeffrey
Formato: pictorial review statistics Journal Article
Publicado: Springer Nature May2016
Acceso en línea:Ver este registro en EBSCOhost
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      pub: Springer Nature
      place: New York, New York
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        atl: Tubular atrophy in the pathogenesis of chronic kidney disease progression.
      aug:
        au: Schelling, Jeffrey
      sug:
        subj:
          Kidney Failure, Chronic Therapy
          Disease Progression
          Nephritis, Interstitial Pathology
          Epithelial Cells Physiopathology
          Child
          Apoptosis
          Oxidative Stress
          Child: 6-12 years
      ab: The longstanding focus in chronic kidney disease (CKD) research has been on the glomerulus, which is sensible because this is where glomerular filtration occurs, and a large proportion of progressive CKD is associated with significant glomerular pathology. However, it has been known for decades that tubular atrophy is also a hallmark of CKD and that it is superior to glomerular pathology as a predictor of glomerular filtration rate decline in CKD. Nevertheless, there are vastly fewer studies that investigate the causes of tubular atrophy, and fewer still that identify potential therapeutic targets. The purpose of this review is to discuss plausible mechanisms of tubular atrophy, including tubular epithelial cell apoptosis, cell senescence, peritubular capillary rarefaction and downstream tubule ischemia, oxidative stress, atubular glomeruli, epithelial-to-mesenchymal transition, interstitial inflammation, lipotoxicity and Na/H exchanger-1 inactivation. Once a a better understanding of tubular atrophy (and interstitial fibrosis) pathophysiology has been obtained, it might then be possible to consider tandem glomerular and tubular therapeutic strategies, in a manner similar to cancer chemotherapy regimens, which employ multiple drugs to simultaneously target different mechanistic pathways.
      pubtype: Academic Journal
      doctype:
        pictorial
        review
        statistics
        Journal Article
      ougenre: Article
    language: English
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