An observational study in Renal Transplant, Renin-Angiotensin System and Rejection Acute Renal, sponsored by Wake Forest University Health Sciences. Completed at 1 site in United States. Open to participants aged 1 Year to 20 Years. Per ClinicalTrials.gov, last updated 2017-11-08.
Sponsored by Wake Forest University Health Sciences · Observational
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.
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.
This is an observational study with a convenience sample of patients recruited from Lucile Packard Children's Hospital kidney transplant evaluation clinic.
Exclusion Criteria:
Kidney transplantation and biomarkers that can identify injury after transplant.
Acute graft injury
Renal biopsy-confirmed acute renal allograft injury as determined by a pathologist (binary yes or no)
Time frame: Within six months after kidney transplant
Chronic graft damage
Renal biopsy-confirmed chronic renal allograft damage as determined by a quantitative fibrosis pathology stain (percent fibrosis from 0 to 100%)
Time frame: Six months after kidney transplant
Renal function
Glomerular filtration rate by the Schwartz equation (mL/min/1.73 m\^2)
Time frame: Within six months after kidney transplant
Proteinuria
Urine protein-to-creatinine ratio above 0.2 mg/mg creatinine
Time frame: Within six months after kidney transplant
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Wake Forest University Health Sciences