Anatomy and function of the ureterovesical opening is briefly described and an etiological classification of vesico-ureteral reflux (VUR) given. The author describes clinical aspects of the reflux and its role in the pathogenesis of pyelonephritis, its course and its action on the upper urinary tract. Animal experimentation was carried out to see if it were possible to cause VUR by bladder inflammation and by what mechanism, and, further, the effect of the vesical inflammation on the upper urinary passages and the role of the VUR in it. In Experiment I bladder infection was caused by insertion of a piece of plastic with simultaneous introduction of bacteria. Experiment II was a repetition of the experiments of Auer and Seager. Here, artificial edema produced a VUR. Experiment III included infiltration of the posterior bladder wall with bacteria to produce severe vesical and ureteral inflammation. Based on these experiments, the author came to the following conclusions: 1. Acute bladder inflammation does not produce VUR if the vesicoureteral valve is normal. 2. The experiments of Auer and Seager are unsuitable models for the ‘inflammatory’ reflux. 3. A well closing ureterovesical valve protects against ascending bacterial movement. 4. If there is a VUR and simultaneous bladder infection, ascending infection practically always results. 5. If inflammation has progressed to the lower ureter, ascending infection follows even without VUR. 6. Since inflammation does not make a normal valve insufficient and most adult sufferers with pyelonephritis do not show VUR, it must be assumed that their renal malady came about in other fashion.

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