One animal experiment suggested that ureteral contraction could be reversibly inhibited by bacteria in the ureteral lumen(6). Moreover, 55–70% of spontaneous rhythmic contractions in sheep ureters were inhibited by the addition of small amounts of growth supernatants from E. coli, Pseudomonas aeruginosa and Klebsiella pneumoniae(13). In our observation, in the case of UVJO combined with febrile UTIs, the degree of ureteral dilatation and the APD during UTI were both higher than the values one week after infection recovery. Ureteropelvic dilatation was relieved after the infection was cured. Similar results were observed in clinical patients and in animal experiments.
Another animal study demonstrated that the combination of infection and obstructive hydronephrosis caused renal pelvic pressure elevation that was higher than that associated with either infection or obstructive hydronephrosis alone(7). In our observation, in the case of UPJO combined with febrile UTIs, the degree of APD during UTI was higher than the values one week after infection recovery. The effect of UTI on the aggravation of hydronephrosis due to UPJO has been demonstrated in clinical patients. However, in the case of UPJO, only the influence of infection on the APD was observed, while the ureter, which was not originally dilated, did not expand under the influence of infection.
There are studies on the mechanism of UTI affecting the upper urinary tract. Flagella and flagellum-mediated motility/chemotaxis contribute to the fitness of uropathogenic E. coli and therefore significantly enhance the pathogenesis of UTIs caused by uropathogenic E. coli (14). E. coli impair ureteric contractility in a Ca-dependent manner, largely caused by the stimulation of potassium channels, and this mechanism is dependent on host-urothelium interactions(15). The second messenger Ca2+ activates the Ca2+/calmodulin-dependent myosin light chain kinase-dependent phosphorylation of 20-kDa regulatory light chains of myosin, which leads to ureteric contraction. Inflammatory factors can initiate spontaneous activity in the proximal and distal ureter(16).
Many animal experiments and mechanisms of infection inhibiting ureteral peristalsis and causing urinary tract dilatation have been studied. The novelty of this study is that urinary tract expansion of UPJO or UVJO patients complicated by febrile UTIs was found to be lower after the infection was cured than during the infection. The clinical significance is described below.
When UPJO or UVJO leads to dilatation of the upper urinary tract, some patients may heal spontaneously, while others may require surgery. One of the surgical indications is a progressive increase in upper urinary tract hydronephrosis during follow-up(2). Febrile UTI is unpleasant but can be quickly controlled with accurate diagnosis and timely treatment. In patients with febrile UTIs, the dilatation of the upper urinary tract was reduced after antibacterial treatment. Therefore, if febrile UTI is present, the influence of UTI should be taken into account in the evaluation of the degree of upper urinary tract dilation to make a more comprehensive surgical decision.
It would be even better to obtain ultrasound values of hydronephrosis within a short period of time (e.g., 1 week) before febrile UTI. We can analyze the dynamic changes in ultrasound results before, during, and after febrile urinary tract infection. However, it is impossible to precisely predict, in advance, which patients will develop febrile UTI. This is clinically challenging. In addition, this was a single-center retrospective study, and the number of single-center cases was not large. If prospective studies can be conducted to obtain the degree of upper urinary tract dilation before, during, and after infection recovery and to obtain more cases, the influence of urinary tract infection on upper urinary tract dilation will be further clarified.