INTRODUCTION AND OBJECTIVES: The mechanism underlying the evolution of congenital obstructive hydronephrosis in humans is still unclear. In previous study we have shown that it is possible to create renal lesions in newborn mice specific to partial ureteral obstruction. We aimed to study the long-term results of such partial obstruction.

METHODS: Mice were operated on the third day of life. We created 2 groups, namely partial unilateral ureteral obstruction (embedding the ureter in the psoas muscle), and controls. We studied pelvis diameter, anter-posterior, kidney length and volume on magnetic resonance imaging (MRI) at day 10 and 3 months postoperatively. Mice were sacrified at 3 months (adult age). We assessed ureter permeability by injecting patented blue into the pelvis. Kidney weight, inflammation and fibrosis on histological assessment were done. â-catenine was used as fibrosis precursor marker, and fibrosis was studied with Sirius red coloration and morphometry.

RESULTS: Magnetic resonance imaging showed parenchyma atrophy in the partially obstructed kidney and compensatory hypertrophy of the controlateral kidney. The pelvis dilatation was already detected at day 10 but it remained stable without significant increase at the 3 months study. The permeability test confirmed the absence of total obstruction on long-term. There was no correlation between the degree of dilatation and parenchyma atrophy or the controlateral hypertrophy. Pathological studies revealed fibrosis in the parenchyma without significant correlation with pelvis dilatation

CONCLUSIONS: Long term results confirmed that partial ureteral obstruction in newborn mice produces irreversible lesions of renal parenchyma. These lesions were not correlated with the dilatation of the upper tract at long term MRI and pathological studies. These results could contribute to the clinical management of obstructive uropthy in children, emphasizing that follow up with simple evaluation of upper tract dilatation is insufficient to predict renal deterioration.

Source of Funding: none