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Objectives: 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.

We investigated the effect of urinary tract infection on bladder and renal pelvic urodynamics in a rat model to examine the role of pressure during infection. Either an antibiotic solution (control group) or Escherichia coli with type 1 pili (infected group) was instilled into the bladder. After 2 to 6 days simultaneous continuous bladder and renal pelvic pressures were measured during urinary flows from less than 2 to greater than 20 ml./kg. per hour while the bladder filled and emptied. Bladder pressures from 50 to 100% of maximum capacity and maximum voiding pressures were significantly higher in the infected group than the control group (36.7 +/- 6.79 cm. water versus 25.5 +/- 5.21 cm. water, respectively, p less than 0.0001). Renal pelvic pressures were significantly higher in the infected group during bladder filling at all urinary flows examined and actually exceeded bladder pressure for the highest flows. We conclude that elevated renal pelvic pressures may contribute to renal changes observed during urinary tract infection.

Disorders of bladder function characterized by physiological urethral obstruction were identified in nearly 50% of patients with non-specific epididymitis and anatomically normaly urinary tracts. This association supports the concept that reflux of urine into the ejaculatory ducts may occur and produce epididymitis. The pathophysiology of retrograde urination is reviewed and the predisposing conditions are discussed.

Residual urine volume (RUV) has been measured in 70 schoolgirls with asymptomatic bacteriuria using 121I-hippuran. The mean volume of residual urine was 23.7 ml. More than 5 ml RUV, the highest value found in 14 girls without bacteriuria or a history of urinary tract infection, was found in 47% of the patients. The mean volume for residual urine in the control girls was 1-1 ml. Among the 44 girls cured for their bacteriuria be a bladder wash out test or antibiotic treatment, recurrence was significantly more common (p less than 0.001) in those greater than 5 ml in RUV (45/20, 75%) than in those with less than or equal to 5 ml (4/24, 17%). In 5 of 22 patients not treated, the bacteriuria disappeared spontaneously during a one year observation period. The RUV was less than 3 ml in 4 of these 5 girls. While the presence of residual urine per se may not be the primary event leading to bacteriuria, it may increase the risk of recurrences, by facilitating bacterial growth and impairing the wash out of bacteria from the bladder on micturition.

Significant bacteriuria (viable count greater than or equal to 10(5)/ml) was found on single testing in 10% of 400 consecutive diabetic women aged 15-65 yr routinely attending a diabetic clinic. Twenty patients with and 21 without significant bacteriuria were then randomly selected for measurement of cardiovascular autonomic reflexes, bladder ultrasound, and mictiography. There were no significant differences between these two groups in age, duration and type of diabetes, glycosylated hemoglobin, blood urea, and creatinine. Abnormalities of cardiovascular autonomic function were more common in the bacteriuric group (P less than .01). Although the bacteriuric group voided a smaller volume of urine, none had evidence of increased residual bladder volume of urine on ultrasound. Diabetic women with cardiovascular autonomic neuropathy appear to be at increased risk of developing bacteriuria. However, age is probably the most important factor influencing the prevalence of bacteriuria in diabetic and in nondiabetic women.