Research & Evidence

Evidence brief: Urinary tract infections, risk factors and antimicrobial resistance patterns in heart failure patients on sodium-glucose transporter 2 inhibitors: Evidence from Jakaya Kikwete Cardiac Institute in Tanzania

A sourced PLOS One study, published 2026-03-26. Read the researchers’ findings, methods and context, with links to connected African health evidence.

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Illustrative stock photograph from Unsplash. It does not depict the reported event, study participants or a confirmed Kenyan facility. Source: https://images.unsplash.com/photo-1579684385127-1ef15d508118

Published in PLOS One on 2026-03-26, this study is presented as an attributed evidence briefing. The excerpts below are the original researchers’ words, reproduced under their Creative Commons Attribution licence. Health Signal has selected the abstract and, where needed, opening background paragraphs; the complete methods, results, limitations and references remain in the linked paper.

Original authors: Julieth Kaaya, Martine A. Manguzu, Deus Buma, Hamu Mlyuka, Samwel Rweyemamu, Albert Ntukula, Helfrid B. Ilomo, Elias Bukundi, Raphael Sangeda, Ritah F. Mutagonda

Source: PLOS One • DOI 10.1371/journal.pone.0344986

Read the complete primary study ↗ · Creative Commons Attribution licence

From the researchers

Abstract

Sodium-glucose co-transporter 2 (SGLT2) inhibitors such as dapagliflozin and empagliflozin are increasingly used in heart failure (HF) management due to their cardiovascular benefits. However, glycosuria induced by SGLT2 inhibition may increase the risk of urinary tract infections (UTIs). Limited data exist on UTI burden among HF patients on SGLT2 inhibitors in low-resource settings.

This study aimed to determine the prevalence of UTIs, associated factors, and antimicrobial susceptibility patterns of uropathogens in HF patients receiving SGLT2 inhibitors at the Jakaya Kikwete Cardiac Institute (JKCI) in Tanzania.

A hospital-based cross-sectional study was conducted from March to June 2024 among HF patients aged ≥18 years on SGLT2 inhibitors. Data was collected using structured questionnaires and medical records. Midstream clean-catch urine samples were collected in sterile containers and processed using semi-quantitative urine culture on CLED and blood agar and subjected to antimicrobial susceptibility testing using the Kirby-Bauer disk diffusion method per CLSI M100 (2024) guidelines. Descriptive statistics and modified Poisson regression were used for analysis.

Out of 138 urine samples processed, 22 (15.9%) showed significant growth. The most common uropathogen was Escherichia coli (50.0%), followed by Klebsiella pneumoniae (13.6%), Pseudomonas aeruginosa (9.1%), and Candida spp. (9.1%). Significant risk factors for UTI included age > 60 years (aPR 3.77; 95% CI: 1.42–10.01), female sex (aPR 2.92; 95% CI: 1.19–7.15), and SGLT2 inhibitor use ≥ 4 months (aPR 3.19; 95% CI: 1.70–5.96). High resistance was observed among bacterial isolates against ampicillin (100%), tetracycline (69.2%), and ceftazidime (53.8%), whereas high susceptibility was noted against nitrofurantoin (84.6%) and meropenem (100%).

UTIs are common among HF patients on SGLT2 inhibitors, with E. coli as the predominant pathogen and a concerning resistance to commonly used antibiotics. These findings underscore the need for routine urine culture and sensitivity testing to guide appropriate therapy and promote antimicrobial stewardship, particularly in resource-constrained settings.

Background

Sodium-glucose co-transporters (SGLT2) inhibitors, including Dapagliflozin, Empagliflozin, Canagliflozin, and Sotagliflozin, are a class of oral antihyperglycemic agents that lower blood glucose by inhibiting its reabsorption in the proximal tubule [1]. In addition to their glucose-lowering effect, SGLT2 inhibitors have demonstrated significant cardiovascular and renal benefits, including reductions in blood pressure, hospitalization for heart failure, and cardiovascular mortality [2]. These findings have led to expanded use beyond diabetes, particularly in the management of heart failure with reduced ejection fraction (HFrEF), where they are now recommended as part of guideline-directed medical therapy [3].

Despite these therapeutic advantages, SGLT2 inhibitors have been associated with an increased risk of genitourinary infections [4]. The mechanism is attributed to induced persistent glucosuria, which creates a glucose-rich urinary environment that may facilitate microbial growth and proliferation [1,4]. This issue warrants particular attention among patients with heart failure, who frequently possess additional predisposing factors for UTI, including comorbidities, impaired immune function, and frequent hospitalization [5]. Furthermore, UTIs in individuals with HF can exacerbate clinical symptoms, precipitate decompensation, and prolong hospitalization, highlighting the need for timely diagnosis and prevention [6]

Reading this evidence

Use the full paper to check the study design, participant selection, comparator and outcome definitions before drawing a practical conclusion. An association does not by itself show cause and effect. A reported performance measure needs its denominator and uncertainty. A finding from a particular facility, sample or time period should retain that scope when it is discussed elsewhere.

This briefing makes the source accessible within the wider research & evidence desk. It does not assess an individual patient or certify a product. When considering relevance to another health system, examine the original authors’ account of context and limitations, then seek local implementation evidence. The related reporting below provides other studies to read alongside this one; it is a topic connection, rather than a claim that their results are directly comparable.

© 2026 Julieth Kaaya, Martine A. Manguzu, Deus Buma, Hamu Mlyuka, Samwel Rweyemamu, Albert Ntukula, Helfrid B. Ilomo, Elias Bukundi, Raphael Sangeda, Ritah F. Mutagonda. Excerpts reproduced under CC BY. Selection, formatting and contextual notes by Health Signal. The researchers are the authors of the source study, not members of Health Signal’s staff.

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Health Signal’s publication desk curates source-based health analysis and attributed research briefings. Study authors and originating institutions are credited within each article. Preparation used AI assistance; source and licence checks do not constitute independent replication or clinical endorsement.

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