AMNIOTIC FLUID STEM CELLS AND CHRONIC KIDNEY DISEASE

Aim: Alport Syndrome (AS) is characterized by a hereditary form of glomerulonephritis, wherein an abnormal level of glomerular basement membrane is produced, gradually leading to interstitial fibrosis and eventual loss of renal function. At present, there is no definitive therapy to delay progression of renal failure. Current therapeutic options are limited to ACE inhibitors, dialysis and eventually transplantation, with end result that is far from being adequate. Stem-cell based therapies may provide alternative therapeutic opportunities. In this study we evaluate the role of amniotic fluid stem cells (AFSC) in a mouse model of AS. Methods: AFSC were administered and blood and urine samples were analyzed for renal function. Kidneys were harvested at different time points and processed for histologic and molecular evaluation. Results: Injected animals presented increased life span and lower albuminuria, creatinine and BUN along with lower levels of inflammatory cytokines. AFSC stimulated activation of M2 macrophages, involved in tissue remodelling. While preserving podocyte number, AFSC do not differentiate into podocytes and do not stimulate production of collagen IVa5, suggesting a paracrine/endocrine mechanism of action through modulation of the renin-angiotensin system. Conclusions: AFSC are capable of slowing down the progression of AS by incurring structural and functional benefits to the kidney. These cells may present an alternative approach to treat medical conditions where currently therapeutic options are either limited or inadequate.