title: Effect of urinary tract infection on ureteropelvic junction obstruction in a rat model.
abstract: OBJECTIVE
  When a partially obstructed kidney becomes infected, more rapid and extreme renal parenchymal damage appears to occur than might result from either infection or obstruction alone. Previously, we showed that either bacteriuria or partial obstruction in congenital unilateral hydronephrosis causes elevated renal pelvic pressures in a rat model. In this same model, we examined the combined effects of partial upper tract obstruction and bacteriuria on renal pelvic and bladder pressures.
  
  
  METHODS
  Female rats from an inbred colony in which more than one half are born with unilateral obstructive hydronephrosis were studied. Type 1 piliated Escherichia coli was instilled into the bladder. Two to 6 days later, the bladder and renal pelvic pressures were measured during varying urinary flows (less than 2 to more than 30 mL/kg/hr). All animals were killed and the kidneys and bladder grossly and histologically assessed. Hydronephrosis was determined at pathologic examination.
  
  
  RESULTS
  Eight rats had congenital unilateral hydronephrosis; five were normal. Acute inflammation was found in all bladder and renal specimens. In hydronephrotic, infected kidneys, the renal pelvic pressures exceeded those in nonhydronephrotic, infected kidneys at all urinary flow rates. Bladder capacity and pressures did not differ between the two groups.
  
  
  CONCLUSIONS
  This model demonstrates that the combination of infection and obstructive hydronephrosis in this model causes renal pelvic pressure elevation that is higher than that associated with either infection or obstructive hydronephrosis alone. These data demonstrate the compound effect that infection and obstruction may have on the kidney and offers an explanation for why this clinical situation is more likely to be associated with greater renal parenchymal injury than either alone.
authors.affiliation: Department of Urology, Stanford University School of Medicine, Stanford, California, USA.
authors.forename: Moritz H
authors.initials: MH
authors.lastname: Hansen
authors.forename: Bing-Yin
authors.initials: BY
authors.lastname: Wang
authors.forename: Naveed
authors.initials: N
authors.lastname: Afzal
authors.forename: Frank G
authors.initials: FG
authors.lastname: Boineau
authors.forename: John E
authors.initials: JE
authors.lastname: Lewy
authors.forename: Linda M D
authors.initials: LM
authors.lastname: Shortliffe
mesh_terms: D000818:Animals; D001437:Bacteriuria / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D006869:Hydronephrosis / Q000151:congenital* / Q000503:physiopathology*; D007674:Kidney Diseases / Q000209:etiology / Q000503:physiopathology; D007682:Kidney Pelvis / Q000503:physiopathology*; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D014517:Ureteral Obstruction / Q000503:physiopathology; D001743:Urinary Bladder / Q000503:physiopathology*; D014552:Urinary Tract Infections / Q000503:physiopathology*; D014563:Urodynamics