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Urinary Tract Infections Management / Diabetes Treatment and Management · Journal article
Reports — Medical Cases Images and Videos · September 1, 2026
Raises a question worth testing. It does not answer one.
This case report documents a single 72-year-old man on dapagliflozin who developed a localized, multidrug-resistant Morganella morganii UTI in the setting of incomplete ureteral duplication, benign prostatic hyperplasia, and urinary stasis. The authors describe a temporal association but explicitly state causality remains unproven and multifactorial, positioning the case as hypothesis-generating rather than evidence of SGLT2 inhibitor causation.
Case report. A 72-year-old man with type 2 diabetes on dapagliflozin, benign prostatic hyperplasia, and incomplete right ureteral duplication with distal fusion (single bladder insertion without dilatation or obstruction). At one month before SGLT2 initiation: prostate ~50 cm³, post-void residual 0 mL, negative…. Intervention: Dapagliflozin 10 mg/day for 4 months prior to presentation; meropenem 1 g IV every 8 hours for 10 days; transurethral resection of prostate 28 days after presentation..
Morganella morganii cultured at 1 × 10^5 CFU/mL in pure culture from midstream specimen Organism resistant to ampicillin, amoxicillin–clavulanate, ampicillin–sulbactam, ceftriaxone, ceftazidime, gentamicin and trimethoprim–sulfamethoxazole; susceptible to piperacillin–tazobactam, levofloxacin/norfloxacin, cefepime and carbapenems Post-void residual increased from 0 mL one month before SGLT2 initiation to ~100 mL at presentation
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This case highlights the importance of culture-guided therapy for multidrug-resistant UTI and individualized clinical judgment regarding SGLT2 inhibitor continuation in patients with urinary stasis or anatomic variants. However, it does not establish a definitive causal link and should not change practice; it raises questions for further investigation.
A single case report describing temporal association between SGLT2 inhibition, anatomic variants, and multidrug-resistant UTI; the authors explicitly state causality is unproven and the narrative is hypothesis-generating.
As stated by the source record.
Quoted from the source exactly as published.
This case highlights the importance of culture-guided therapy for multidrug-resistant UTI and individualized clinical judgment regarding SGLT2 inhibitor continuation in patients with urinary stasis or anatomic variants. However, it does not establish a definitive causal link and should not change practice; it raises questions for further investigation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background and Clinical Significance: Sodium–glucose cotransporter-2 (SGLT2) inhibitors cause persistent glucosuria, which has been hypothesized to facilitate urinary tract infection (UTI) when urinary stasis or anatomic variants coexist; causality, however, remains unproven and almost certainly multifactorial. Case Presentation: A 72-year-old man treated with dapagliflozin 10 mg/day for 4 months presented with 3 days of dysuria and nocturia, without fever or systemic signs. One month before SGLT2 inhibitor initiation, urological work-up had been unremarkable: prostate ~50 cm3, post-void residual (PVR) 0 mL, and a negative midstream culture. At presentation we obtained a midstream clean-catch specimen before antibiotics. Dipstick showed glucose 2+ (~100 mg/dL, as expected with SGLT2 inhibition), leukocyte esterase 3+ and nitrites negative; microscopy revealed 45 leukocytes/high-power field with pronounced bacteriuria. Quantitative culture grew Morganella morganii at 1 × 105 CFU/mL in pure culture. Antimicrobial susceptibility (VITEK® 2 Compact, EUCAST v14.0, 2024) demonstrated resistance to ampicillin, amoxicillin–clavulanate, ampicillin–sulbactam, ceftriaxone, ceftazidime, gentamicin and trimethoprim–sulfamethoxazole, with susceptibility (S) retained only to piperacillin–tazobactam, levofloxacin/norfloxacin, cefepime and carbapenems (ertapenem, meropenem). Imaging revealed a right duplicated ureter with distal fusion (single bladder insertion, no dilatation or obstruction) and benign prostatic hyperplasia with PVR ~100 mL; renal function was preserved, two blood culture sets (pre-antibiotic) were negative, and repeat urine culture on day 7 was sterile. Management/outcome: The episode was classified as a localized (cystitis-range) UTI per European Association of Urology (EAU) criteria (no fever, flank pain or bacteremia). Meropenem 1 g intravenously every 8 h (3 g/day) was given for 10 days after urology/infectious-disease review. Dapagliflozin was held at presentation and not restarted during the 3-month follow-up period; reintroduction was planned only after full urological reassessment with cardiology input. Transurethral resection of the prostate (TUR-P) was performed 18 days after completing antibiotics (28 days after presentation) for bladder outlet obstruction refractory to tamsulosin 0.4 mg daily, with complete resolution of symptoms, normalization of inflammatory markers and PVR 0 mL. No recurrence occurred during 3 months of follow-up after TUR-P. Conclusions: This single case illustrates a temporal association—not proven causation—between SGLT2-related glucosuria, incomplete emptying and a non-obstructive duplicated ureter that likely created a permissive milieu for opportunistic Morganella UTI. The narrative is hypothesis-generating; urinary stasis was the dominant modifiable factor. Culture-guided therapy, individualized decisions on SGLT2 continuation, and definitive correction of outlet obstruction are the practical takeaways.
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