Kidney growth,hypertrophy and the unifying mechanism of diabetic complications |
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Authors: | J Satriano |
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Institution: | (1) Division of Nephrology-Hypertension, Department of Medicine, The Veterans Administration San Diego Healthcare System, University of California San Diego, San Diego, CA, USA;(2) The Stein Institute for Research on Aging, University of California, San Diego, CA, USA |
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Abstract: | Summary. Michael Brownlee has proposed a ‘Unifying Mechanism’ of hyperglycemia-induced damage in diabetes mellitus. At the crux of
this hypothesis is the generation of reactive oxygen species (ROS), and their impact on glycolytic pathways.
Diabetes is the leading cause of chronic kidney failure. In the early phase of diabetes, prior to establishment of proteinuria
or fibrosis, comes kidney growth and hyperfiltration. This early growth phase consists of an early period of hyperplasia followed
by hypertrophy. Hypertrophy also contributes to cellular oxidative stress, and may precede the ROS perturbation of glycolytic
pathways described in the Brownlee proposal. This increase in growth promotes hyperfiltration, and along with the hypertrophic
phenotype appears required for hyperglycemia-induced cell damage and the progression of downstream diabetic complications.
Here we will evaluate this growth phenomenon in the context of diabetes mellitus. |
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Keywords: | : Type I diabetes – Hyperfiltration – Tubuloglomerular feedback – Reactive oxygen species – Polyamines – Hypertrophy |
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