Endothelial Damage, Inflammation and Immunity in Chronic Kidney Disease

Maribel Diaz-Ricart1,2,3, Sergi Torramade-Moix1,2, Georgina Pascual4

  • 1Hematopathology, Pathology Department, Center for Biomedical Diagnosis (CDB), Hospital Clinic, 08036 Barcelona, Spain.

Toxins
|June 5, 2020
PubMed

Insights

Chronic kidney disease (CKD) accelerates atherosclerosis and thrombotic risks. Uremic endothelial cells link inflammation and immunity defects in CKD patients, contributing to disease progression.

Area of Science:

  • Nephrology
  • Cardiovascular Science
  • Immunology

Background:

  • Chronic kidney disease (CKD) patients exhibit accelerated atherosclerosis and higher risks of thrombotic-ischemic events and mortality.
  • Endothelial damage in CKD is linked to a proinflammatory state, oxidative stress, and toxin accumulation from impaired renal clearance.
  • Uremic endothelial cells are implicated in and affected by innate immunity activation.

Purpose of the Study:

  • To review the connection between endothelial damage, inflammation, and defective immunity in uremia.
  • To explore the role of uremic endothelial cells in the immune response within CKD.

Main Methods:

  • Literature review focusing on the mechanisms of endothelial dysfunction in CKD.
  • Analysis of the interplay between innate immunity activation and endothelial cells in uremic environments.
  • Examination of danger-associated molecular patterns (DAMPs) and their signaling pathways.

Main Results:

  • Uremic endothelial cells produce DAMPs, activating pattern recognition receptors.
  • This activation leads to increased adhesion molecules, proinflammatory cytokines, and reactive oxygen species in endothelial cells.
  • These processes establish a link between immunity and inflammation in the context of uremia.

Conclusions:

  • Endothelial damage, inflammation, and immune dysfunction are interconnected in CKD.
  • Uremic endothelial cells play a central role in mediating these pathological connections.
  • Understanding these links is crucial for managing thrombotic complications and mortality in CKD.

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