In this study, we attempted to determine whether there are differences between CRF and non-CRF patients in the bacteriologic patterns of community-acquired APN or in the antibiotic sensitivity patterns of uropathogens. This study showed that CRF does not seem to influence the isolation rates of different uropathogens or their susceptibility patterns to antimicrobials in patients with community-acquired APN that presented as a positive urine culture.
In general, CRF patients are known to be vulnerable to infection due to weakened immunity . But little information is available regarding the role of CRF as a risk factor for the development of antimicrobial resistance in uropathogens. It has been reported that DM per se does not seem to influence the isolation rates of different uropathogens or their susceptibility patterns to antimicrobials . In this study, the antimicrobial susceptibilities of microorganisms isolated in cases of community-acquired APN in non-DM and DM groups did not differ. However, the role of CRF in the etiology and antimicrobial resistance of uropathogens in patients with community-acquired APN has not been clarified.
It is known that E. coli is isolated in approximately 90% of APN cases . Other studies have found that urinary Klebsiella is more frequent in diabetic patients compared to the detection rate in non-diabetic patients [16, 17]. In this study, the most common cause of APN was E. coli (58.3%, 293 cases), followed by K. pneumoniae (12.7%, 64 cases). Due to the inclusion of diabetic patients, K. pneumoniae was more common than in previous reports on APN. Among the microorganisms associated with APN, E. coli was found in 54.8% and 65.7% of cases in the non-CRF group and CRF group, respectively (p = NS), and K. pneumonia was present in 12.2% and 13.9% of cases, respectively (p = NS). There were no differences between the groups regarding the rates of other APN microorganisms.
In a previous analysis of the antibiotic sensitivity of E. coli in APN, the sensitivities to the first- and third-generation cephalosporins, aminoglycoside and ciprofloxacin were greater than 90%; 47% to ampicillin; and 60% to TMP-SMX . In our current study, the rate of E. coli sensitivity was 96.9% to imipenem, 99.2% to amikacin, 90.8% to tobramycin, greater than 80% to third- and fourth-generation cephalosporin antibiotics, 71.7% to ciprofloxacin, and 61.4% to TMP-SMX. However, the sensitivity rates to gentamycin and ampicillin were low (42.9% and 39.4%, respectively). Little data is available on the role of CRF as a risk factor for the development of antimicrobial resistance in uropathogens. Antimicrobial sensitivities to ampicillin in the non-CRF group and CRF group were 37.8% and 20.0%, respectively (p = 0.024), and those to gentamycin in the non-CRF group and CRF group were 71.9% and 51.9%, respectively (p = 0.016). The antimicrobial sensitivities to other antibiotics did not differ between the two groups. In North America, a cut-off point of 20% has been suggested as the level of resistance at which an agent should no longer be used . The observed high rates of E. coli resistance to ampicillin, cephalothin, and gentamycin precludes, at least in our area, the choice of these or similar drugs in the empirical initial treatment of community-acquired APN in CRF and non-CRF patients.
In a recent case-control study, recent hospitalization and fluoroquinolone use in the previous six months were independent risk factors for fluoroquinolone resistance in community-onset febrile E. coli UTI . In our study, we excluded cases of previous administration of antibiotics and hospital-acquired APN.
Recent cohort studies have suggested that CRF is also a risk factor for non-cardiovascular morbidity  and mortality, including those caused by infection [22, 23]. Few studies have investigated the associations between CRF and specific infectious conditions. In this study, the value of HS-CRP was 7.0 (± 7.8) mg/dL in the non-CRF group and 11.0 (± 9.4) mg/dL in the CRF group (p = 0.002). The values of WBC (p = 0.001) and ESR (p = 0.03) were higher in the CRF group than they were in the non-CRF group. Based on these results, we propose that patients with CRF had higher values of inflammatory markers when they had APN and that more attention is needed in this area because community-acquired APN in CRF patients can be a serious illness.
The limitations of our study include performance on non-CRF and CRF patients admitted to a single hospital, although the study included a large number of patients. Second, the CRF group was older in age than was the non-CRF group. Finally, the results for blood culture were not included in this study.
Based on our results, ampicillin, cephalothin, and gentamycin should not be considered as an initial therapeutic regimen in either CRF or non-CRF patients with community-acquired APN. In our series of patients with community-acquired APN presenting with a positive urine culture test, CRF per se does not seem to influence the isolation rates of different uropathogens or their susceptibility patterns to antimicrobials. A detailed prospective study is required to address the influences of CRF on the spectrum and antimicrobial susceptibility of the uropathogens involved in community-acquired APN.