Background/Objectives: Recurrent urinary tract infection (rUTI) is common after menopause, but estrogen deficiency alone does not explain variation in recurrence, symptoms, and microbial profiles. This study aimed to synthesize evidence on the interactions among estrogen deficiency, urogenital microbial ecology, diabetes, obesity, microbial reservoirs, and anatomical, neurological, and functional modifiers of postmenopausal rUTI susceptibility. Methods: PubMed and Scopus were searched for original studies published from 1 January 2021 to 15 June 2026. A structured narrative synthesis included 62 original reports comprising clinical interventions, observational cohorts, microbiome and multi-omic studies, and cellular and animal experiments. Evidence was interpreted according to study design, population relevance, and biological directness. Results: Menopause was associated with reduced Lactobacillus dominance, higher vaginal pH, and altered vaginal or urinary communities, although findings were heterogeneous. Vaginal estrogen reduced recurrence and improved the local urogenital environment, but microbiome restoration is not established as its sole mechanism. Gut, rectal, vaginal, urinary, and bladder-wall reservoirs may contribute to persistence or repeated exposure. Diabetes was linked to dysbiosis and impaired urothelial defence, whereas obesity evidence remained less direct. Pelvic organ prolapse with incomplete emptying, elevated postvoid residual urine, age-related detrusor dysfunction, stroke, immobility, functional dependence, incontinence, and catheter exposure may further modify susceptibility. Conclusions: Postmenopausal rUTI is multifactorial. The urogenital microbiome–metabolic interface is a useful integrative framework, but not a validated causal or diagnostic model. Vaginal estrogen, urine culture, metabolic and bladder-function assessment, and antimicrobial stewardship remain the clinical foundation; microbiome-directed strategies require prospective validation.