BACKGROUND

Many diseases lead to renal failure, and chronic kidney disease remains a global health threat. No matter what the underlying disease, fibrosis, or “non-reversible scarring,” is the most important reason why End Stage Renal Failure (ESRF) occurs. Currently, the treatment of chronic kidney disease is centered on slowing its progression and reducing co-morbidities. The only currently available therapies include those that reduce hypertension, proteinuria, hyperlipidemia, hyperglycemia or the renin-angiotensin-aldosterone feedback system. Unfortunately, these therapies do not prevent ESRF for the majority of patients.

TECHNOLOGY DESCRIPTION

The inventors have shown that AFSCs can ameliorate
glycerol-induced acute tubular necrosis (ATN) in animals. They demonstrated that the main mechanism by which AFSCs are renal-protective in ATN is through a significant immunomodulatory effect.

They also demonstrated that injection of AFSCs is renoprotective (protects the kidney from progressive disease) in Alport syndrome mouse models. Mice injected with AFSCs demonstrated improved kidney morphology (including preservation of glomerular and tubular structures), as well as the restoration to normal of creatinine, BUN
levels and glomerular filtration rate. In addition, treated mice showed an increased life span, thus slowing down the progression of the disease.

They have developed a proprietary methodology and know-how for extracting, characterizing and culturing AFSCs and renal progenitor cells from human amniotic fluid.

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File Number: 2008-018 

Web site: http://www.chla.org/site/c.ipINKTOAJsG/b.474061...

Disease: Kidneys and Genito-Urinary System

Other Information:

Principal Investigator:
David Warburton

Additional Investigator(s):
Laura Perin, Roger E. De Filippo

Contact
Jessica L. Rousset, Director
Email: JRousset@chla.usc.edu
Phone: 323.361.4531