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Renal Function in Diabetic Disease Models: The Tubular System in the Pathophysiology of the Diabetic Kidney

Diabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a patho... Full description

Journal Title: Annual review of physiology 2012, Vol.74 (1), p.351-375
Main Author: Vallon, Volker
Other Authors: Thomson, Scott C
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: United States: Annual Reviews, Inc
ID: ISSN: 0066-4278
Link: https://www.ncbi.nlm.nih.gov/pubmed/22335797
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3807782
title: Renal Function in Diabetic Disease Models: The Tubular System in the Pathophysiology of the Diabetic Kidney
format: Article
creator:
  • Vallon, Volker
  • Thomson, Scott C
subjects:
  • Animals
  • Article
  • Cell cycle
  • Cell growth
  • Development and progression
  • Diabetes
  • Diabetic nephropathies
  • Diabetic Nephropathies - metabolism
  • Diabetic Nephropathies - pathology
  • Diabetic Nephropathies - physiopathology
  • diabetic nephropathy
  • Disease Progression
  • Electrolytes - metabolism
  • Feedback, Physiological
  • Glomerular filtration rate
  • Glomerular Filtration Rate - physiology
  • glomerular hyperfiltration
  • Glucose - metabolism
  • Glucose Transport Proteins, Facilitative - metabolism
  • Glucose Transporter Type 2 - metabolism
  • Humans
  • Hypertrophy
  • Kidney Glomerulus - metabolism
  • Kidney Glomerulus - physiopathology
  • Kidney Tubules - metabolism
  • Kidney Tubules - pathology
  • Kidney Tubules - physiopathology
  • Kidney Tubules, Proximal - pathology
  • Kidneys
  • Kinases
  • Risk factors
  • Sodium - metabolism
  • Sodium Chloride - metabolism
  • sodium-glucose cotransport
  • tubular growth
  • tubular transport
  • urogenital system
  • Usage
ispartof: Annual review of physiology, 2012, Vol.74 (1), p.351-375
description: Diabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a pathophysiological concept that focuses on the tubular system to explain these changes. The concept includes the tubular hypothesis of glomerular filtration, which states that early tubular growth and sodium-glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the physiology of tubuloglomerular feedback. The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-β and cyclin-dependent kinase inhibitors causes a cell cycle arrest and a switch to tubular hypertrophy and a senescence-like phenotype. Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0066-4278
fulltext: fulltext
issn:
  • 0066-4278
  • 1545-1585
url: Link


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descriptionDiabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a pathophysiological concept that focuses on the tubular system to explain these changes. The concept includes the tubular hypothesis of glomerular filtration, which states that early tubular growth and sodium-glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the physiology of tubuloglomerular feedback. The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-β and cyclin-dependent kinase inhibitors causes a cell cycle arrest and a switch to tubular hypertrophy and a senescence-like phenotype. Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.
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languageeng
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subjectAnimals ; Article ; Cell cycle ; Cell growth ; Development and progression ; Diabetes ; Diabetic nephropathies ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Diabetic Nephropathies - physiopathology ; diabetic nephropathy ; Disease Progression ; Electrolytes - metabolism ; Feedback, Physiological ; Glomerular filtration rate ; Glomerular Filtration Rate - physiology ; glomerular hyperfiltration ; Glucose - metabolism ; Glucose Transport Proteins, Facilitative - metabolism ; Glucose Transporter Type 2 - metabolism ; Humans ; Hypertrophy ; Kidney Glomerulus - metabolism ; Kidney Glomerulus - physiopathology ; Kidney Tubules - metabolism ; Kidney Tubules - pathology ; Kidney Tubules - physiopathology ; Kidney Tubules, Proximal - pathology ; Kidneys ; Kinases ; Risk factors ; Sodium - metabolism ; Sodium Chloride - metabolism ; sodium-glucose cotransport ; tubular growth ; tubular transport ; urogenital system ; Usage
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descriptionDiabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a pathophysiological concept that focuses on the tubular system to explain these changes. The concept includes the tubular hypothesis of glomerular filtration, which states that early tubular growth and sodium-glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the physiology of tubuloglomerular feedback. The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-β and cyclin-dependent kinase inhibitors causes a cell cycle arrest and a switch to tubular hypertrophy and a senescence-like phenotype. Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.
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abstractDiabetes mellitus affects the kidney in stages. At the onset of diabetes mellitus, in a subset of diabetic patients the kidneys grow large, and glomerular filtration rate (GFR) becomes supranormal, which are risk factors for developing diabetic nephropathy later in life. This review outlines a pathophysiological concept that focuses on the tubular system to explain these changes. The concept includes the tubular hypothesis of glomerular filtration, which states that early tubular growth and sodium-glucose cotransport enhance proximal tubule reabsorption and make the GFR supranormal through the physiology of tubuloglomerular feedback. The diabetic milieu triggers early tubular cell proliferation, but the induction of TGF-β and cyclin-dependent kinase inhibitors causes a cell cycle arrest and a switch to tubular hypertrophy and a senescence-like phenotype. Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy.
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