Kidney endothelial dysfunction

Ischemia, localized infections and sepsis

Bruce Molitoris, Ruben M. Sandoval

Research output: Chapter in Book/Report/Conference proceedingChapter

9 Citations (Scopus)

Abstract

Endothelial cells play a key role in initiating and propagating the inflammatory response seen in ischemia, infections and sepsis. Situated in a key position between the epithelial cells and white blood cells (WBC), they interact and respond to signals from both cell types. Microvascular endothelial cells within the kidney mediate coagulation, WBC attachment, WBC migration into the interstitium, microvascular flow rates and permeability. Low regeneration potential and endothelial-mesenchymal transformation lead to fibrosis and subsequent microvascular dropout. This last event is in large part responsible for a chronic reduction in regional perfusion, subsequent increased vulnerability to recurrent acute kidney injury, and acceleration of chronic kidney disease progression to end-stage renal disease. Glomerular endothelial dysfunction may lead to preglomerular shunting of blood flow allowing kidney blood flow to remain close to normal while resulting in a reduction in glomerular filtration rate.

Original languageEnglish
Title of host publicationContributions to Nephrology
Pages108-118
Number of pages11
Volume174
DOIs
StatePublished - Sep 2011

Publication series

NameContributions to Nephrology
Volume174
ISSN (Print)03025144

Fingerprint

Sepsis
Leukocytes
Ischemia
Kidney
Endothelial Cells
Infection
Glomerular Filtration Rate
Chronic Renal Insufficiency
Acute Kidney Injury
Chronic Kidney Failure
Cell Movement
Disease Progression
Regeneration
Permeability
Fibrosis
Perfusion
Epithelial Cells

ASJC Scopus subject areas

  • Nephrology

Cite this

Molitoris, B., & Sandoval, R. M. (2011). Kidney endothelial dysfunction: Ischemia, localized infections and sepsis. In Contributions to Nephrology (Vol. 174, pp. 108-118). (Contributions to Nephrology; Vol. 174). https://doi.org/10.1159/000329248

Kidney endothelial dysfunction : Ischemia, localized infections and sepsis. / Molitoris, Bruce; Sandoval, Ruben M.

Contributions to Nephrology. Vol. 174 2011. p. 108-118 (Contributions to Nephrology; Vol. 174).

Research output: Chapter in Book/Report/Conference proceedingChapter

Molitoris, B & Sandoval, RM 2011, Kidney endothelial dysfunction: Ischemia, localized infections and sepsis. in Contributions to Nephrology. vol. 174, Contributions to Nephrology, vol. 174, pp. 108-118. https://doi.org/10.1159/000329248
Molitoris B, Sandoval RM. Kidney endothelial dysfunction: Ischemia, localized infections and sepsis. In Contributions to Nephrology. Vol. 174. 2011. p. 108-118. (Contributions to Nephrology). https://doi.org/10.1159/000329248
Molitoris, Bruce ; Sandoval, Ruben M. / Kidney endothelial dysfunction : Ischemia, localized infections and sepsis. Contributions to Nephrology. Vol. 174 2011. pp. 108-118 (Contributions to Nephrology).
@inbook{a2b59c943b95457a9ce32ba1dd53e6ce,
title = "Kidney endothelial dysfunction: Ischemia, localized infections and sepsis",
abstract = "Endothelial cells play a key role in initiating and propagating the inflammatory response seen in ischemia, infections and sepsis. Situated in a key position between the epithelial cells and white blood cells (WBC), they interact and respond to signals from both cell types. Microvascular endothelial cells within the kidney mediate coagulation, WBC attachment, WBC migration into the interstitium, microvascular flow rates and permeability. Low regeneration potential and endothelial-mesenchymal transformation lead to fibrosis and subsequent microvascular dropout. This last event is in large part responsible for a chronic reduction in regional perfusion, subsequent increased vulnerability to recurrent acute kidney injury, and acceleration of chronic kidney disease progression to end-stage renal disease. Glomerular endothelial dysfunction may lead to preglomerular shunting of blood flow allowing kidney blood flow to remain close to normal while resulting in a reduction in glomerular filtration rate.",
author = "Bruce Molitoris and Sandoval, {Ruben M.}",
year = "2011",
month = "9",
doi = "10.1159/000329248",
language = "English",
isbn = "9783805598101",
volume = "174",
series = "Contributions to Nephrology",
pages = "108--118",
booktitle = "Contributions to Nephrology",

}

TY - CHAP

T1 - Kidney endothelial dysfunction

T2 - Ischemia, localized infections and sepsis

AU - Molitoris, Bruce

AU - Sandoval, Ruben M.

PY - 2011/9

Y1 - 2011/9

N2 - Endothelial cells play a key role in initiating and propagating the inflammatory response seen in ischemia, infections and sepsis. Situated in a key position between the epithelial cells and white blood cells (WBC), they interact and respond to signals from both cell types. Microvascular endothelial cells within the kidney mediate coagulation, WBC attachment, WBC migration into the interstitium, microvascular flow rates and permeability. Low regeneration potential and endothelial-mesenchymal transformation lead to fibrosis and subsequent microvascular dropout. This last event is in large part responsible for a chronic reduction in regional perfusion, subsequent increased vulnerability to recurrent acute kidney injury, and acceleration of chronic kidney disease progression to end-stage renal disease. Glomerular endothelial dysfunction may lead to preglomerular shunting of blood flow allowing kidney blood flow to remain close to normal while resulting in a reduction in glomerular filtration rate.

AB - Endothelial cells play a key role in initiating and propagating the inflammatory response seen in ischemia, infections and sepsis. Situated in a key position between the epithelial cells and white blood cells (WBC), they interact and respond to signals from both cell types. Microvascular endothelial cells within the kidney mediate coagulation, WBC attachment, WBC migration into the interstitium, microvascular flow rates and permeability. Low regeneration potential and endothelial-mesenchymal transformation lead to fibrosis and subsequent microvascular dropout. This last event is in large part responsible for a chronic reduction in regional perfusion, subsequent increased vulnerability to recurrent acute kidney injury, and acceleration of chronic kidney disease progression to end-stage renal disease. Glomerular endothelial dysfunction may lead to preglomerular shunting of blood flow allowing kidney blood flow to remain close to normal while resulting in a reduction in glomerular filtration rate.

UR - http://www.scopus.com/inward/record.url?scp=82755161223&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=82755161223&partnerID=8YFLogxK

U2 - 10.1159/000329248

DO - 10.1159/000329248

M3 - Chapter

SN - 9783805598101

VL - 174

T3 - Contributions to Nephrology

SP - 108

EP - 118

BT - Contributions to Nephrology

ER -