Abstract
Congenital urinary tract obstruction is an important cause of renal disease in children. Early animal studies have shown a relationship between the timing of obstruction and the different pathological entities that collectively comprise renal maldevelopment. A multitude of molecular factors through both in-vivo and in-vitro studies have been identified that are involved in apoptosis and/or interstitial fibrosis as a result of urinary tract obstruction. These molecular factors have been found to work in parallel and also occasionally divergent pathways. Apoptosis is a prominent feature of early in-utero urinary tract obstruction and a major factor in the loss of renal mass and renal dysfunction. Furthermore, there is an increasing body of evidence to suggest that apoptosis is an inciting event in the development of progressive interstitial fibrosis which further contributes to renal demise. Clearly, a better understanding of the mechanisms of apoptosis and the subsequent development of targeted therapies directed against apoptosis may prove beneficial in the prevention of renal dysfunction associated with urinary tract obstruction.
Keywords: Apoptosis, interstitial fibrosis, obstruction, nephropathy, cystic dysplasia, hydronephrosis, renal tubular cells, Osteopontin, Angiotensin II, urinary tract
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