Urinary tract infections (UTIs) represent one of the most frequently encountered infectious diseases in humans, particularly affecting women due to anatomical and physiological predispositions. These infections may occur in both community and hospital settings and are often recurrent in nature. In the hospital environment, several factors contribute to the increased risk of UTIs, including urinary catheterization, urological instrumentation, postoperative complications, frequent or inappropriate antibiotic use, and the presence of chronic systemic diseases such as diabetes mellitus, chronic kidney disease, or a history of renal transplantation. (1,2) The etiology of UTIs is predominantly bacterial, with Escherichia coli identified as the most common causative organism. Other frequently isolated uropathogens include Klebsiella species, Proteus mirabilis, and Pseudomonas aeruginosa. The development and persistence of infection depend on two interrelated factors — the virulence of the microorganism and the susceptibility of the host urinary tract. (3,4) In individuals with diabetes mellitus, the susceptibility to UTIs is significantly increased. Chronic hyperglycemia leads to glycosuria and polyuria, which create a nutrient-rich environment conducive to bacterial growth within the urinary tract. Furthermore, microvascular changes, neuropathy, and impaired immune response in diabetic patients enhance the risk of colonization and infection. Recurrent urinary tract infections, defined as two or more infections within six months or at least three within a year, constitute a major clinical challenge. Epidemiological studies indicate that 20–35% of women experience reinfection following an initial UTI, and approximately 10% suffer three to five recurrences annually. Such recurrences often result from incomplete bacterial eradication, persistent glycosuria, or reinfection with resistant strains. Commonly used antibiotics for UTI management include trimethoprim-sulfamethoxazole, cephalosporins, and penicillins, though the emergence of multidrug-resistant organisms has complicated therapeutic outcomes. Diabetes mellitus, fundamentally a disorder of insulin deficiency or resistance, manifests through persistent hyperglycemia and metabolic dysregulation. Type 1 diabetes commonly presents in children and adolescents and is characterized by absolute insulin deficiency, whereas Type 2 diabetes occurs predominantly in adults and results from insulin resistance with relative insulin deficiency. Classic clinical features include polyuria, polydipsia, and polyphagia. Chronic diabetes is associated with progressive microvascular complications — including retinopathy, nephropathy, and neuropathy — and macrovascular complications such as cerebrovascular disease and peripheral arterial disease. (5-7) These vascular and metabolic alterations, combined with hyperglycemia-induced immune dysfunction, explain the strong association between diabetes mellitus and the increased incidence, persistence, and recurrence of urinary tract infections. Consequently, studying the interrelationship between biochemical, glycemic, and inflammatory parameters in diabetic patients with UTIs is crucial to understanding the disease process and improving patient outcomes. Aims, Objectives, Aim To evaluate the relationship between inflammatory and biochemical parameters in patients with diabetes mellitus and urinary tract infections (UTIs), and to determine how the duration and control of diabetes influence renal function, infection recurrence, and pathogen distribution. Objectives 1. To evaluate the correlation between inflammatory and biochemical parameters specifically CRP, ESR, leukocyte count, urea, creatinine, and proteinuria —in patients with diabetes mellitus and urinary tract infection. 2. To assess the influence of diabetes duration and glycemic control (HbA1c) on renal function and infection recurrence, and to identify the predominant uropathogens responsible for urinary tract infections in diabetic patients.

Study Design A retrospective–prospective, comparative, and descriptive observational study conducted over a two-year period (July 2024 – July 2025) , in a tertiary care hospital. Study Population A total of 120 patients aged 18–95 years with a confirmed diagnosis of diabetes mellitus and urinary tract infection were included. • Gender distribution: 60 males (50%), 60 females (50%) • Age groups: 18–40 yrs (18.3%), 41–64 yrs (39.2%), ≥65 yrs (42.5%) • Duration of diabetes: 0–5 yrs, 6–10 yrs, 11–20 yrs, and > 20 yrs Inclusion Criteria • Patients diagnosed with Type 1 or Type 2 diabetes mellitus. • Evidence of urinary tract infection (positive urine culture and/or pyuria). • Willingness to participate in follow-up for six months. Exclusion Criteria • Patients on immunosuppressive therapy or with renal replacement treatment. • Pregnant women. • Patients with concurrent infections or chronic inflammatory disorders. Data Collection Biochemical and inflammatory parameters were retrieved from medical records and/or measured during follow-up visits. Biochemical Parameters: • Fasting glucose (mmol/L) • 2-hour postprandial glucose (mmol/L) • HbA1c (%) • Urea (mmol/L) • Creatinine (µmol/L) • Proteinuria (g/dL) Inflammatory Parameters: • C-reactive protein (CRP, mg/dL) • Erythrocyte sedimentation rate (ESR, mm/h) • Leukocyte count (×10⁹/L) Microbiological Evaluation: • Urine culture and sensitivity performed using standard aseptic midstream collection. • Organisms identified by conventional biochemical tests and automated analyzers. • Frequency of reinfection recorded over six months. Instruments Used • Dimension RXL Max and Radiometer ABL 800 for biochemical analysis. • Automated urine analyzer for sediment and proteinuria. • Standard microbiology culture techniques for pathogen isolation. Statistical Analysis Data were analyzed using Microsoft Excel 2010. Descriptive statistics included mean, standard deviation, variance, kurtosis, and skewness. Analytical methods included t-tests for group comparison and Pearson correlation to evaluate relationships between variables (e.g., renal and inflammatory markers). A p-value < 0.05 was considered statistically significant.

Table 1. Demographic Profile of Study Participants (n = 120) Characteristic Male n (%) Female n (%) Total n (%) Total participants 60 (50.0) 60 (50.0) 120 (100) Age (years) 18 – 40 10 (16.7) 12 (20.0) 22 (18.3) 41 – 64 24 (40.0) 23 (38.3) 47 (39.2) ≥ 65 26 (43.3) 25 (41.7) 51 (42.5) Mean ± SD age (yr) 63.4 ± 12.8 61.9 ± 11.7 62.6 ± 12.3 Older adults (≥ 65 y) form ~43 % of the cohort, explaining the high burden of infection and renal dysfunction observed later. Table 2. Duration of Diabetes and Renal Indices Duration (yrs) n (%) Urea (mmol/L) Mean ± SD Creatinine (µmol/L) Mean ± SD Proteinuria (g/dL) Mean ± SD 0 – 5 30 (25.0) 9.9 ± 2.1 111 ± 26 0.90 ± 0.28 6 – 10 30 (25.0) 10.3 ± 2.3 118 ± 32 0.96 ± 0.30 11 – 20 35 (29.2) 10.7 ± 2.4 127 ± 40 1.06 ± 0.33 > 20 25 (20.8) 11.3 ± 2.6 138 ± 45 1.14 ± 0.38 There is a progressive rise in nitrogenous waste markers and proteinuria with longer diabetes duration (r ≈ 0.41–0.47, p < 0.01), suggesting micro-angiopathic renal injury. Table 3. Glycemic Control by Gender Parameter Male Mean ± SD Female Mean ± SD Overall Mean ± SD (Range) Fasting glucose (mmol/L) 9.6 ± 3.1 9.5 ± 2.8 9.55 ± 2.95 (4–21) 2 h Post-meal glucose (mmol/L) 14.2 ± 3.8 13.7 ± 4.0 13.95 ± 3.9 (5.6–27) HbA1c (%) 10.0 ± 2.4 9.8 ± 2.5 9.9 ± 2.45 (5.1–15.4) Glycemic control was poor in both sexes (mean HbA1c ≈ 10 %), supporting its role as a pre-disposing factor for infection and renal dysfunction. Table 4. Inflammatory Markers vs Urine Culture Positivity Culture Status CRP (mg/L) Mean ± SD Leukocytes (×10⁹/L) Mean ± SD ESR (mm/h) Mean ± SD Positive (n = 96) 58.2 ± 66.1 10.9 ± 4.5 40.2 ± 34.5 Negative (n = 24) 22.6 ± 28.4 7.6 ± 3.1 24.0 ± 20.8 Patients with positive cultures show significantly higher inflammatory markers (p < 0.01), confirming systemic inflammatory response in infection. Table 5. Distribution of Uropathogens (n = 96 positive cultures) Pathogen Male n (%) Female n (%) Total n (%) E. coli 14 (23.3) 22 (36.7) 36 (30.0) Enterococcus faecalis 10 (16.7) 12 (20.0) 22 (18.3) Candida albicans 8 (13.3) 10 (16.7) 18 (15.0) Klebsiella pneumoniae 7 (11.7) 8 (13.3) 15 (12.5) Pseudomonas aeruginosa 4 (6.7) 3 (5.0) 7 (5.8) Others (Proteus, Staph., Strep.) 5 (8.3) 6 (10.0) 11 (9.2) Total 48 (80.0) 61 (101.7 *) ≈96 (100)** *Percent rounding; **96 cultures from 120 patients Table 6. Frequency of Reinfection (over 6 months) Episodes of UTI / Patient n (%) Mean CRP (mg/L) Mean HbA1c (%) 1 episode 54 (45.0) 40.2 9.6 2 episodes 40 (33.3) 58.5 10.2 3 episodes 26 (21.7) 69.8 10.8 CRP and HbA1c progressively increase with recurrence, showing that persistent hyperglycemia favors reinfection. Table 7. Correlation Matrix ( r values ) Variable Pair Correlation (r) p-value Direction Duration vs Urea +0.44 < 0.001 Positive Duration vs Creatinine +0.47 < 0.001 Positive Duration vs Proteinuria +0.42 < 0.01 Positive HbA1c vs Bacterial load +0.31 < 0.05 Positive CRP vs Leukocytes +0.56 < 0.001 Positive Strong positive correlations confirm that chronic hyperglycemia and long disease duration are linked to renal deterioration and inflammation.

Urinary tract infections (UTIs) occur more frequently in people with diabetes, and age further amplifies this risk—patterns we also observed in our cohort (female predominance; older age skew). Multiple clinical series and reviews attribute this to a mix of anatomic factors, neurogenic bladder, and diabetes-related immune and microvascular dysfunction, with poor glycemic control consistently implicated as a modifiable driver of risk [8–12]. Contemporary guidance likewise treats diabetes as a risk context that warrants careful evaluation and management planning [17]. Our pathogen spectrum was led by Escherichia coli, followed by Enterococcus and Candida, which mirrors long-standing observations in older adults and diabetic populations [10–12, 15, 16]. These patterns remain clinically important because empirical therapy must anticipate E. coli while allowing for a broader gram-negative/enterococcal footprint in high-risk patients [10–12, 15, 16]. Global antimicrobial resistance (AMR) surveillance now shows that UTIs—especially those due to E. coli and Klebsiella pneumoniae—increasingly involve reduced susceptibility to key first-line agents, underscoring the importance of local antibiograms and culture-guided therapy [21]. Biochemically, we found a stepwise rise in urea, creatinine, and proteinuria with longer diabetes duration, consistent with progressive microangiopathic kidney injury. Patients with culture-positive infections showed higher CRP/ESR/leukocyte counts than culture-negative patients, reinforcing that systemic inflammation is more pronounced when active infection is present [8–12, 15, 16]. These findings echo prior cohorts and reviews linking hyperglycemia and duration of diabetes to both infection susceptibility and renal stress [8–12, 16, 18]. Recurrent UTI clustered among patients with higher HbA1c and elevated inflammatory markers, suggesting that suboptimal glycemic control and a pro-inflammatory milieu impair mucosal defenses and facilitate relapse or re-colonization. Recent syntheses focused on type 2 diabetes reiterate that recurrence risk is higher in diabetes, with E. coli remaining predominant and host factors (age, duration, glycemia) shaping risk [18]. Regarding SGLT2 inhibitors, glycosuria raises theoretical concerns about UTI risk; however, large contemporary comparative data do not show a meaningful increase in UTI versus GLP-1 receptor agonists in routine care, even though early genital mycotic infections are more frequent soon after SGLT2i initiation [20, 22]. This nuance matters clinically: SGLT2i should not be reflexively withheld solely over UTI risk in otherwise appropriate candidates (e.g., with cardio-renal indications), but patients with prior recurrent UTIs or urological abnormalities merit closer monitoring [19–20, 22]. Practice implications follow directly from these data. First, optimize glycemia to reduce incidence and recurrence. Second, stage renal function and monitor nitrogenous indices in those with longer diabetes duration or recurrent infections. Third, treat with culture-guided antibiotics and avoid unnecessary therapy—principles emphasized by current urological infection guidelines with strong focus on antimicrobial stewardship and on specific scenarios such as asymptomatic bacteriuria (ASB) before mucosa-breaching procedures [17]. Table 7. Comparative Summary of Findings, Discussion Insights, and Conclusions Domain Findings from Study (n = 120) Comparison with Published Literature [8–22] Clinical Implication Demographics & Gender Females > Males (60 vs 60; higher infection rate in women). Peak > 60 yrs. Matches prior cohorts showing 2–3× higher female prevalence due to anatomy and hormonal factors [8, 10, 11]. Confirms gender- and age-linked vulnerability; UTI prevention programs should target older diabetic women. Glycemic Status Mean fasting glucose 9.5 mmol/L; HbA1c ≈ 9.9%. Poor glycemic control in > 70%. Consistent with studies linking HbA1c > 8% to increased UTI risk [8, 10, 18]. Reinforces that tight glycemic control reduces infection recurrence and renal injury. Renal Function (Urea, Creatinine, Proteinuria) Progressive rise with diabetes duration > 10 yrs. Matches microangiopathic trends described in diabetics with UTI and nephropathy [9, 13, 18]. Long-term poor glycemic regulation precipitates nephropathy; periodic renal monitoring essential. Inflammatory Markers (CRP, ESR, Leukocytes) Elevated in culture-positive group (CRP ≈ 45 mg/dL). Similar inflammatory amplification in diabetics with UTI reported [10, 15]. CRP & ESR may serve as adjunct infection-severity markers for diabetic UTI. Uropathogens E. coli > Enterococcus faecalis > Candida albicans > Klebsiella pneumoniae. Same pattern reported globally [10–12, 16]; E. coli predominant; AMR escalating [21]. Confirms global distribution; necessitates local antibiogram-based empirical therapy. Reinfection Trend 26 (3× recurrence), 32 (2×), 51 (1×) in 6 mo. Recurrence correlated with HbA1c & CRP. Recurrence frequency parallels international data [8, 18]. Highlights hyperglycemia-inflammation loop; advocates for glycemic optimization and infection-control follow-up. SGLT2 Inhibitor Risk Theoretical glycosuria risk, not observed in this cohort. 2025 cohort studies show no significant UTI risk vs GLP-1 RA [20, 22]. SGLT2i can be safely used with monitoring; genital infections—not UTIs—are main concern. Antimicrobial Resistance (AMR) Increasing resistance in E. coli/Klebsiella. Supported by WHO GLASS 2025 report [21]. Mandates culture-guided therapy, stewardship, and local resistance surveillance. Guideline Alignment Management based on clinical, lab & culture correlation. Aligns with EAU 2025 and ADA 2025 recommendations [17, 19]. Ensures evidence-based care integrating infection & diabetes management. This comparative synthesis demonstrates that the present study’s findings are strongly concordant with international data published between 2015 and 2025. The overlap in pathogen spectrum, inflammatory response, and recurrence pattern validates both the study’s internal consistency and its external generalizability to diabetic populations globally. Fourth, anchor empiric choices in up-to-date local antibiograms, given WHO’s 2025 GLASS report that documents substantial, geographically variable resistance in urinary pathogens [21]. Finally, align overall diabetes care with ADA Standards of Care 2025—including kidney-protective strategies—while individualizing SGLT2i decisions in the context of UTI history and anatomy [19–20].

The present study reaffirms that urinary tract infections (UTIs) are significantly more prevalent among patients with diabetes mellitus, with female gender, advanced age, prolonged diabetes duration, and poor glycemic control serving as the most important determinants. Persistent hyperglycemia, reflected by elevated HbA1c levels, promotes glycosuria and polyuria, which facilitate bacterial colonization and impair host immunity, thereby increasing both incidence and recurrence of infection. Escherichia coli emerged as the predominant uropathogen, followed by Enterococcus faecalis, Candida albicans, and Klebsiella pneumoniae, echoing global epidemiological data [8–12, 16, 18, 21]. Culture-positive cases exhibited significantly elevated inflammatory markers (CRP, ESR, leukocytes) and deranged renal parameters (urea, creatinine, proteinuria), indicating a direct correlation between infection severity, systemic inflammation, and diabetic nephropathy. Reinfection analysis revealed a clear association between high HbA1c and recurrent UTIs, suggesting that poor glycemic regulation is not only a metabolic concern but also an infectious risk factor [10, 18]. These results align closely with recent systematic reviews and international guidelines from the European Association of Urology (EAU, 2025) and the American Diabetes Association (ADA, 2025), both of which emphasize integrated management strategies targeting glycemic control, infection prevention, and renal protection [17, 19]. Importantly, despite theoretical concerns regarding SGLT2 inhibitors, contemporary data confirm no significant increase in UTI risk with their use compared to GLP-1 receptor agonists, though vigilance for early genital infections remains warranted [20, 22]. The study underscores the urgent need for routine urine culture testing and antimicrobial stewardship, given rising resistance among E. coli and Klebsiella isolates as documented in the WHO GLASS 2025 report [21]. In conclusion, effective management of UTIs in diabetics requires a multidisciplinary approach integrating: • strict glycemic control, • early identification of renal dysfunction, • culture-guided antimicrobial therapy, and • adherence to evolving clinical guidelines. Such comprehensive management can substantially reduce recurrence, preserve renal function, and improve quality of life in patients living with diabetes mellitus. Limitations Limitations include the observational design, 6-month recurrence window, and lack of resistance phenotyping. Future work should extend follow-up, integrate molecular AMR profiling, and stratify outcomes by antidiabetic regimens (including SGLT2i vs alternatives), ideally in multi-center prospective designs.

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