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Clinical Trial Summary

Endothelial progenitor cells that reside in renal vasculature may be stimulated to initiate differentiation programs during episodes of injury. It is hypothesized that endothelial progenitor cells resident in the kidney can transition to a post-injury phenotype that promotes endothelial repair.


Clinical Trial Description

Endothelial dysfunction is central to the pathophysiology of vascular ischemia, bacterial sepsis, toxin-induced thrombotic microangiopathy, and antibody-mediated kidney transplant rejection and often manifest with renal failure. With each of these diagnoses circulating components of the complement cascade bind to endothelial cells and induce disease progression through anaphylactic cellular messaging, monocyte homing, and direct cell membrane disruption. In response to injury during embryologic development avascular metanephric blastema initiate endothelial differentiation. Although circulating hematopoietic progenitor cells have shown therapeutic promise they incorporate into renal vasculature at very low density. ;


Study Design


Related Conditions & MeSH terms


NCT number NCT04896567
Study type Interventional
Source Brigham and Women's Hospital
Contact
Status Withdrawn
Phase Phase 1
Start date January 21, 2022
Completion date December 30, 2024

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