Molecular mechanisms of Diabetic kidney disease

Kimberly J. Reidy, Hyun Mi Kang, Thomas Hostetter, Katalin Susztak

Research output: Contribution to journalArticle

228 Citations (Scopus)

Abstract

Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide and the single strongest predictor of mortality in patients with diabetes. DKD is a prototypical disease of gene and environmental interactions. Tight glucose control significantly decreases DKD incidence, indicating that hyperglycemia-induced metabolic alterations, including changes in energy utilization and mitochondrial dysfunction, play critical roles in disease initiation. Blood pressure control, especially with medications that inhibit the angiotensin system, is the only effective way to slow disease progression. While DKD is considered a microvascular complication of diabetes, growing evidence indicates that podocyte loss and epithelial dysfunction play important roles. Inflammation, cell hypertrophy, and dedifferentiation by the activation of classic pathways of regeneration further contribute to disease progression. Concerted clinical and basic research efforts will be needed to understand DKD pathogenesis and to identify novel drug targets.

Original languageEnglish (US)
Pages (from-to)2333-2340
Number of pages8
JournalJournal of Clinical Investigation
Volume124
Issue number6
DOIs
StatePublished - Jun 2 2014

Fingerprint

Diabetic Nephropathies
Disease Progression
Cell Dedifferentiation
Podocytes
Angiotensins
Diabetes Complications
Hyperglycemia
Hypertrophy
Renal Insufficiency
Regeneration
Blood Pressure
Inflammation
Glucose
Mortality
Incidence
Research
Pharmaceutical Preparations
Genes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Molecular mechanisms of Diabetic kidney disease. / Reidy, Kimberly J.; Kang, Hyun Mi; Hostetter, Thomas; Susztak, Katalin.

In: Journal of Clinical Investigation, Vol. 124, No. 6, 02.06.2014, p. 2333-2340.

Research output: Contribution to journalArticle

Reidy, KJ, Kang, HM, Hostetter, T & Susztak, K 2014, 'Molecular mechanisms of Diabetic kidney disease', Journal of Clinical Investigation, vol. 124, no. 6, pp. 2333-2340. https://doi.org/10.1172/JCI72271
Reidy, Kimberly J. ; Kang, Hyun Mi ; Hostetter, Thomas ; Susztak, Katalin. / Molecular mechanisms of Diabetic kidney disease. In: Journal of Clinical Investigation. 2014 ; Vol. 124, No. 6. pp. 2333-2340.
@article{0d1af990776842f6a5e0236af6accb4f,
title = "Molecular mechanisms of Diabetic kidney disease",
abstract = "Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide and the single strongest predictor of mortality in patients with diabetes. DKD is a prototypical disease of gene and environmental interactions. Tight glucose control significantly decreases DKD incidence, indicating that hyperglycemia-induced metabolic alterations, including changes in energy utilization and mitochondrial dysfunction, play critical roles in disease initiation. Blood pressure control, especially with medications that inhibit the angiotensin system, is the only effective way to slow disease progression. While DKD is considered a microvascular complication of diabetes, growing evidence indicates that podocyte loss and epithelial dysfunction play important roles. Inflammation, cell hypertrophy, and dedifferentiation by the activation of classic pathways of regeneration further contribute to disease progression. Concerted clinical and basic research efforts will be needed to understand DKD pathogenesis and to identify novel drug targets.",
author = "Reidy, {Kimberly J.} and Kang, {Hyun Mi} and Thomas Hostetter and Katalin Susztak",
year = "2014",
month = "6",
day = "2",
doi = "10.1172/JCI72271",
language = "English (US)",
volume = "124",
pages = "2333--2340",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "6",

}

TY - JOUR

T1 - Molecular mechanisms of Diabetic kidney disease

AU - Reidy, Kimberly J.

AU - Kang, Hyun Mi

AU - Hostetter, Thomas

AU - Susztak, Katalin

PY - 2014/6/2

Y1 - 2014/6/2

N2 - Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide and the single strongest predictor of mortality in patients with diabetes. DKD is a prototypical disease of gene and environmental interactions. Tight glucose control significantly decreases DKD incidence, indicating that hyperglycemia-induced metabolic alterations, including changes in energy utilization and mitochondrial dysfunction, play critical roles in disease initiation. Blood pressure control, especially with medications that inhibit the angiotensin system, is the only effective way to slow disease progression. While DKD is considered a microvascular complication of diabetes, growing evidence indicates that podocyte loss and epithelial dysfunction play important roles. Inflammation, cell hypertrophy, and dedifferentiation by the activation of classic pathways of regeneration further contribute to disease progression. Concerted clinical and basic research efforts will be needed to understand DKD pathogenesis and to identify novel drug targets.

AB - Diabetic kidney disease (DKD) is the leading cause of kidney failure worldwide and the single strongest predictor of mortality in patients with diabetes. DKD is a prototypical disease of gene and environmental interactions. Tight glucose control significantly decreases DKD incidence, indicating that hyperglycemia-induced metabolic alterations, including changes in energy utilization and mitochondrial dysfunction, play critical roles in disease initiation. Blood pressure control, especially with medications that inhibit the angiotensin system, is the only effective way to slow disease progression. While DKD is considered a microvascular complication of diabetes, growing evidence indicates that podocyte loss and epithelial dysfunction play important roles. Inflammation, cell hypertrophy, and dedifferentiation by the activation of classic pathways of regeneration further contribute to disease progression. Concerted clinical and basic research efforts will be needed to understand DKD pathogenesis and to identify novel drug targets.

UR - http://www.scopus.com/inward/record.url?scp=84902195666&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84902195666&partnerID=8YFLogxK

U2 - 10.1172/JCI72271

DO - 10.1172/JCI72271

M3 - Article

VL - 124

SP - 2333

EP - 2340

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 6

ER -