Background: The most common nonlethal congenital anomaly of the urinary tract is ureteral obstruction without dysplasia. Although rarely progressive, the morbidity associated with metabolic and surgical management is considerable. Our study was designed to measure local and systemic pathophysiologic mechanisms in an immature model of chronic partial unilateral ureteral obstruction (UUO) after completion of glomerulogenesis.
Methods: A partial UUO was created by the method of "psoas wrap" in young male weanling rats. Control animals were sham operated. Three groups were divided as follows: sham (N= 15), UUO (N= 18), and UUO + angiotensin-converting enzyme (ACE) (N= 16) inhibitor, enalapril. Renal glomerular and tubular functions were determined by creatinine and uric acid clearances. Diuresis was assessed by urine volume, osmolality, and fractional solute excretions from samples above and below the obstruction. Proteinuria was determined by the urine protein/creatinine ratio (Up/c).
Results: Proteinuria was attenuated in UUO + ACE-treated animals. The hyperuricemia of the immature UUO animals was avoided by an increase in the clearance of uric acid in the UUO + ACE-treated group. Fractional solute excretions suggested a diversion of diuresis to the contralateral unobstructed kidney.
Conclusion: Angiotensin blockade during chronic UUO in young rats affords protection by attenuating proteinuria, promoting uricosuria, and diverting solute diuresis. These data suggest a complex interaction of local and systemic mechanisms unique to the maturing kidney.