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.
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 Type
INTERVENTIONAL
Allocation
NA
Purpose
BASIC_SCIENCE
Masking
NONE
Tissue from kidney biopsy will be used to isolate Cluster Differentiation 34+ cells.
Brigham and Women's Hospital
Boston, Massachusetts, United States
Cell growth
Tissue will be isolated and cell viability will be documented by rate of colony growth over one week per patient enrolled.
Time frame: 1 week
Kidney disease progression
Isolated cell growth will be compared to serum creatinine of patients
Time frame: 3 years
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