Renal Transplant Injury and the Renin-Angiotensin System in Kids (RETASK)
| Status: | Completed |
|---|---|
| Conditions: | Renal Impairment / Chronic Kidney Disease |
| Therapuetic Areas: | Nephrology / Urology |
| Healthy: | No |
| Age Range: | 1 - 20 |
| Updated: | 11/10/2017 |
| Start Date: | July 16, 2014 |
| End Date: | April 26, 2017 |
In pediatric kidney transplant patients, rejection, medication toxicity and ischemia cause
early and chronic renal allograft injury, which reduces graft lifespan and patient survival.
Early detection of injury would facilitate prevention and treatment. The gold standard
surveillance biopsy has limitations including delayed discovery of injury. No noninvasive
test identifies graft injury before it is clinically apparent. This project's goal is to
develop a novel early marker of subclinical graft injury to facilitate prompt recognition and
treatment.
early and chronic renal allograft injury, which reduces graft lifespan and patient survival.
Early detection of injury would facilitate prevention and treatment. The gold standard
surveillance biopsy has limitations including delayed discovery of injury. No noninvasive
test identifies graft injury before it is clinically apparent. This project's goal is to
develop a novel early marker of subclinical graft injury to facilitate prompt recognition and
treatment.
Kidney damage activates the traditional renin-angiotensin (Ang) system (RAS), characterized
by Ang-converting enzyme (ACE)/Ang II/Ang II type 1 receptor. The Ang-converting enzyme 2
(ACE2)/Ang-(1-7)/Mas pathway counteracts this damage. The balance, or ratio, between levels
of the ACE/Ang II and ACE2/Ang-(1-7) pathways may be clinically important because Ang-(1-7)
counteracts Ang II-mediated injury. An increase in ACE and Ang II expression and a decrease
in ACE2 and Ang-(1-7) expression on tubular cells may promote renal injury. Tubular damage
may increase urinary loss of protective ACE2 and Ang-(1-7), propagating renal damage by
allowing ACE and Ang II to stimulate inflammation and fibrosis unopposed. The investigators
hypothesis is that a shift in the urinary ACE-to-ACE2 and Ang II-to-Ang-(1-7) ratios towards
ACE2 and Ang-(1-7) predicts acute graft injury diagnosed on renal biopsy and predicts chronic
graft damage on renal biopsy.
by Ang-converting enzyme (ACE)/Ang II/Ang II type 1 receptor. The Ang-converting enzyme 2
(ACE2)/Ang-(1-7)/Mas pathway counteracts this damage. The balance, or ratio, between levels
of the ACE/Ang II and ACE2/Ang-(1-7) pathways may be clinically important because Ang-(1-7)
counteracts Ang II-mediated injury. An increase in ACE and Ang II expression and a decrease
in ACE2 and Ang-(1-7) expression on tubular cells may promote renal injury. Tubular damage
may increase urinary loss of protective ACE2 and Ang-(1-7), propagating renal damage by
allowing ACE and Ang II to stimulate inflammation and fibrosis unopposed. The investigators
hypothesis is that a shift in the urinary ACE-to-ACE2 and Ang II-to-Ang-(1-7) ratios towards
ACE2 and Ang-(1-7) predicts acute graft injury diagnosed on renal biopsy and predicts chronic
graft damage on renal biopsy.
Inclusion Criteria:
- Ages 1 - 20 years
- Actively listed on the transplant list at Lucile Packard Children's Hospital at
Stanford and received a renal transplant during the study enrollment period
Exclusion Criteria:
- Transplanted at a center other than Lucile Packard Children's Hospital at Stanford
We found this trial at
1
site
1 Medical Center Blvd
Winston-Salem, North Carolina 27103
Winston-Salem, North Carolina 27103
(336) 716-2011
Wake Forest University Baptist Medical Center Welcome to Wake Forest Baptist Medical Center, a fully...
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