Background: Congenital obstructive nephropathy is the principal cause of end stage renal disease (ESRD) in children ( Beneldet al. 2003). Obstructive nephropathy leads to Hydronephrosis, dened clinically by an enlargement of the kidney as a result of urine accumulation in the renal pelvis or calyces. [1,2] Ureteropelvic junction (UPJ) obstruction is the most common cause of hydronephrosis with an estimated incidence of 1 in 1000–1500 newborns ( Changet al. 2004). [2,3] Aims: To evaluate the pathogenesis of congenital ureteropelvic junction obstruction (UPJO) by histopathology, IHC markers CD117 & S100 and special stain Masson's Trichrome. Methods And Materials: The study group consists of 50 Pediatric cases presenting with intrinsic ureteropelvic junction obstruction and 15 patients with Wilms tumor with no UPJO formed the control group. All the cases and controls were subjected to histopathological examination, immunohistochemical staining with markers CD117 & S100 and special stain Masson's Trichrome. Mann – Whitney U test and Pearson's chisquare test were used for statistical analysis. The cases had reduce Results: d CD117 and S100 expression, Irregularity of muscle bers, increased wall thickness & muscle thickness and submucosal collagen deposition compared to controls. Decreased ICC interpreted by Conclusions: decreased CD117, decreased neural innervation interpreted by decreased S100, structural changes - Irregularity of muscle bers arrangement, increased submucosal collagen deposition and increased smooth muscle thickness possibly cause disruption of the mobility of UPJ and lead functional obstruction.
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