Urinary tract infections (UTIs) are among the most common bacterial infections worldwide and are traditionally considered acute and self-limited conditions. However, growing evidence suggests that recurrent or persistent UTIs may contribute to chronic kidney disease (CKD) progression through complex interactions between uropathogens and host responses. This review examines the pathophysiological links of UTIs caused by uropathogenic Escherichia coli, Klebsiella spp., and Enterococcus spp. and the development of chronic renal injury. Pathogen-specific persistence mechanisms, including intracellular survival, biofilm formation, and chronic colonization, may promote sustained inflammation, oxidative stress, and maladaptive repair responses. These processes are associated with tubular injury and progressive fibrotic remodeling. In addition, host-related factors such as diabetes, immune dysfunction, and antimicrobial resistance may further influence disease progression. Emerging biomarkers of inflammation, tubular injury, and fibrosis may improve early detection and risk stratification in patients with recurrent or complicated UTIs. Collectively, these findings support the concept that recurrent UTIs may represent potential contributors to CKD progression in susceptible individuals and highlight the importance of early recognition, pathogen-oriented management, and improved diagnostic strategies.
Caragea et al. (Sun,) studied this question.