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Research Article

Run a risk Factors for Development of Acute Kidney Injury in Patients with Urinary Tract Infection

  • Chih-Yen Hsiao,
  • Huang-Yu Yang,
  • Meng-Chang Hsiao,
  • Peir-Haur Hung,
  • Ming-Cheng Wang

PLOS

x

  • Published: July 27, 2022
  • https://doi.org/10.1371/journal.pone.0133835

Abstruse

Acute kidney injury (AKI) is associated with high morbidity and bloodshed. Urinary tract infection (UTI) may be associated with sepsis or septic shock, and crusade sudden deterioration of renal function. This study investigated the clinical characteristics and change of renal part to place the risk factors for development of AKI in UTI patients. This retrospective study was conducted in a 3rd referral middle. From January 2006 to January 2022, a full of 790 UTI patients necessitating infirmary admission were included for terminal analysis. Their demographic and clinical characteristics and comorbidities were nerveless and compared. Multivariate logistic regression assay was performed to evaluate the risk factors for AKI in UTI patients. There were 97 (12.3%) patients developing AKI during hospitalization. Multivariate logistic regression analysis showed that patients with older age (OR 1.02, 95% CI ane.00–1.04, P = 0.04), diabetes mellitus (DM) (OR 2.23, 95% CI 1.35–3.68, P = 0002), upper UTI (OR ii.63, 95% CI 1.53–iv.56, P = 0001), afebrile during hospitalization (OR 1.71, 95% CI ane.04–2.83, P = 0036) and lower baseline eGFR [baseline eGFR 45–59 mL/min/i.73 m2 (OR two.12, 95% CI i.12–4.04, P = 0.022), baseline eGFR 30-44 mL/min/1.73 m2 (OR 4.44, 95% CI 2.xxx–8.60 P < 0.001) baseline eGFR < thirty mL/min/1.73 chiliad2 (OR 4.72, 95% CI 2.thirteen–x.45, P <0.001), respectively] were associated with increased risk for development of AKI. were associated with increased risk for development of AKI. Physicians should pay attention to UTI patients at adventure of AKI (advancing age, DM, upper UTI, afebrile, and dumb baseline renal function).

Citation: Hsiao C-Y, Yang H-Y, Hsiao Thou-C, Hung P-H, Wang M-C (2015) Risk Factors for Development of Acute Kidney Injury in Patients with Urinary Tract Infection. PLoS I 10(7): e0133835. https://doi.org/10.1371/journal.pone.0133835

Editor: Stanislaw Stepkowski, Academy of Toledo, Usa

Received: January 18, 2022; Accustomed: July 2, 2022; Published: July 27, 2022

Copyright: © 2022 Hsiao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original writer and source are credited

Data Availability: All relevant data are inside the paper and its Supporting Information files.

Funding: The authors have no back up or funding to report.

Competing interests: The authors have alleged that no competing interests be.

Introduction

Urinary tract infection (UTI) is one of the most common bacterial infections [ane]. The overall annual incidence of UTI was i.75% amongst residents of the Calgary Health Region, Canada during 2004–2005 [two]. The 2007 National Ambulatory Medical Care Surveys estimated UTIs were responsible for nearly 2 one thousand thousand visits to emergency departments annually in the United states of america [3].

UTI can be either asymptomatic or symptomatic, characterized by a wide spectrum of symptoms ranging from mild irritative voiding to bacteremia, sepsis, daze or even death. In specific patient groups, urosepsis may show loftier bloodshed rates of 25% to 60% [four].

Sepsis is one of the almost common triggers of acute kidney injury (AKI) [five], and about threescore% patients with septic daze developed AKI [half dozen]. Acute UTI may crusade sudden deterioration of renal function, especially for urinary tract obstacle [7]. AKI is associated with high morbidity and bloodshed during acute care [8–10]. Patients with severe AKI were under increased risk of end stage renal disease and even decease after hospital discharge [11–13].

Since sepsis-related AKI leads to poor outcomes and increased healthcare costs, identification of the risk factors for development of AKI in patients with UTI is disquisitional. However, there were few studies focusing on this important event. In this retrospective study, we investigated the clinical characteristics and modify of renal function to identify the gamble factors for development of AKI in UTI patients.

Materials and Methods

Ideals argument

This retrospective observational study complied with the guidelines of the Proclamation of Helsinki and was approved by the Medical Ethics Committee of Chia-Yi Christian Hospital, a 3rd referral center located in the southwestern function of Taiwan. Since this study involved retrospective review of existing information, blessing from the Institutional Review Board of Chia-Yi Christian Hospital was obtained (Approval # CYCH-IRB-100015), merely without specific informed consent from patients. Furthermore, not only were all data securely protected (by delinking identifying information from the primary data sets) and made available only to investigators, only they were also analyzed anonymously. The Institutional Review Board of Chia-Yi Christian Hospital specifically waived the need for consent for these studies. Finally, all primary information were collected according to procedures outlined in epidemiology guidelines to strengthen the reporting of observational studies.

Study Conduct

This retrospective written report was conducted in a 3rd referral eye located in a metropolis of southern Taiwan with a population of 547,000 people. The hospital has 1,000 acute intendance beds, and serves approximately three,800 outpatients and 260 emergency patients daily. The authors had full access to the results and vouch for the completeness and accuracy of the data and analysis.

Study population

From Jan 2006 to Jan 2022, clinical data of 938 consecutive hospitalized patients with baseline creatinine values diagnosed with UTI in the Chia-Yi Christian Hospital were enrolled. The criteria for the diagnosis of UTI were symptomatic, including pain on urination, lumbago or fever with bacterial isolation of more than than 104 colony forming units (CFU)/mL. Patients with concurrent infections other than UTI or receiving chronic dialysis therapy (i.e., regular dialysis therapy more than iii months) before UTI episode were excluded from this study (Fig ane). Finally a total of 790 patients with UTI were included for analyses.

Infirmary Course

Inpatients were assessed by standard laboratory and diagnostic procedures. Clinical data including age, sex activity, diabetes mellitus (DM), hypertension, coronary artery disease (CAD), congestive heart failure (CHF), cerebrovascular disease, malignancy, and medications such as antihypertensive drugs or nephrotoxic agents (i.east., aminoglycosides, nonsteroidal anti-inflammatory drugs (NSIAD), dissimilarity media, and trimethoprim/sulfamethoxazole) were recorded. Patients admitted were treated with antibiotics based on the standard protocol. The initial regimens of empiric antibody therapy were parenteral commencement generation cephalosporin plus aminoglycoside (if no impaired renal role), parenteral second generation cephalosporin or parenteral fluoroquinolones to treat the common UTI pathogens for patients with stable hemodynamic condition. Parenteral empiric antibiotic therapy according to previous culture results and antimicrobial susceptibility was prescribed for patients with recurrent UTI. Specific antibody therapy was administered co-ordinate to the culture results and antimicrobial susceptibility during hospitalization. The four master vital signs including pulse rate, respiration rate, claret pressure, and temperature were routinely monitored.

Major Outcomes and Definitions.

AKI was diagnosed by a decrease in glomerular filtration rate (GFR) more than fifty% or doubling of serum creatinine compared to that at baseline co-ordinate to The Burglarize GFR criteria [14]. Estimated GFR (eGFR) was adamant according to the Chronic Kidney Illness Epidemiology Collaboration (CKD-EPI) creatinine equation [15]. The baseline level of serum creatinine was obtained at dates 3 months before admission. The diagnosis and classification of chronic kidney disease (CKD) were established co-ordinate to the criteria of the National Kidney Foundation Thou/DOQI Clinical Practise Guidelines for Chronic Kidney Disease [xvi]. Diagnosis of DM was based on the American Diabetes Association and the World Health Arrangement criteria. Upper UTI was an infection of the kidney or ureter; lower UTI included cystitis, urethritis, and prostatitis. Bacteremia was an invasion of the bloodstream by leaner and confirmed by blood culture. Fever was defined as a temperature above 38.three°C (101°F) [17, 18]. Afebrile was defined as UTI patients who did not have a temperature above 38.3°C (101°F). Septic shock was defined every bit sepsis with hypotension (systolic blood pressure less than 90 mmHg or a fall in systolic blood pressure level > 40 mmHg) lasting for at least one hour despite adequate fluid resuscitation [19].

Written report Design

Patients were divided into two groups based on the presence (group 1) or absence (group ii) of AKI during the hospital stay. Demographic data of gender, historic period, co-morbidities (diabetes mellitus, hypertension, CHF, CAD, stroke, and malignancy), upper or lower UTI, baseline renal function, indwelling urinary catheter, vital signs at admission, and presence of bacteremia or septic daze during hospitalization were reviewed from the medical charts and data were collected for further analyzed.

Statistical analysis

Data are expressed as means and standard deviations for continuous variables and as frequency and proportions for categorical variables. Continuous information were analyzed using a Mann-Whitney U-examination. Categorical information were analyzed by Fisher's exact test or chi-square examination. Nosotros performed a conditional logistic regression assay with AKI as the outcome variable and baseline demography as well as clinical relevant data as the chief exposure of interest. A P value under 0.05 was considered pregnant. Statistical analyses were performed by the software SPSS 17.0 (International Business organization Machines Corp., Armonk, NY, The states).

Results

At that place were 790 UTI patients enrolled for concluding analysis, their demographic and clinical characteristics of UTI patients are shown in Table 1. The hateful historic period was 65 ± 18 years, 543 (68.7%) were female. In that location were 335 hypertensive patients, among which 180 were treated with angiotensin-converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs). A full of 47 patients were establish to have urinary tract obstruction. A full of 369 patients were afebrile UTI during hospitalization, and 15 of them had hypothermia. There were 97 patients (12.3%) developing AKI afterward access with 4 patients (0.v%) necessitating dialysis therapy. The overall mortality rate was 0.38% (three/790). Patients who adult AKI had older historic period (72 ± 13 versus 64 ± 19 years, P <0.001) and higher serum creatinine at admission (three.37 ±ane.96 versus 1.32 ± 0.94 mg/dL, P <0.001), college prevalence of DM (56.7% versus 35.6%, P <0.001), hypertension (54.6% versus 40.7%, P = 0.009), upper UTI (46.4% versus 35.5%, P = 0.037), afebrile (59.eight% versus 44.nine%, P = 0.006), septic shock (22.7% versus 9.viii%, P <0.001) and bacteremia (39.two% versus 28.6%, P = 0.033), lower values of systolic and diastolic blood pressure (127 ± 33 versus 137 ± thirty mmHg, and 70 ± 17 versus 77 ± 15 mmHg, P = 0.006 and P <0.001, respectively) and baseline eGFR (53 ± 23 versus 72 ± 27 mL/min/1.73m2, P <0.001), and less exposure to nephrotoxic agents (47.4% versus 69.3%, P <0.001) compared with those without AKI.

In multivariate logistic regression analysis, older historic period (OR 1.02, 95% CI i.00–1.04, P = 0.04), DM (OR 2.23, 95% CI ane.35–3.68, P = 0002), upper UTI (OR ii.63, 95% CI 1.53–iv.56, P = 0001), afebrile during hospitalization (OR i.71, 95% CI ane.04–2.83, P = 0036) and lower baseline eGFR [baseline eGFR 45–59 mL/min/1.73 mii (OR ii.12, 95% CI i.12–4.04, P = 0.022), baseline eGFR 30–44 mL/min/i.73 m2 (OR 4.44, 95% CI 2.30–eight.60 P < 0.001) baseline eGFR < 30 mL/min/ane.73 1000ii (OR four.72, 95% CI 2.13–10.45, P <0.001), respectively] were independently associated with increased risk for development of AKI in patients admitted with UTI (Tabular array 2) (Fig 2).

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Fig 2. Multivariate analysis of associations betwixt eGFR and acute kidney injury.

aN = 790. bMultivariate model adjusted for gender, diabetes mellitus, hypertension, congestive eye failure, coronary artery disease, stroke, malignancy, indwelling foley catheter, afebrile, upper UTI, septic shock, baseline eGFR grouping.

https://doi.org/10.1371/journal.pone.0133835.g002

Discussion

AKI is a mutual complication of sepsis and septic shock. UTI is one of the mutual causes of sepsis and may cause sudden deterioration in renal function. Several studies suggested that AKI was not a mutual complication among patients with acute pyelonephritis [xx–22]. In this study, the incidence of AKI in UTI patient necessitating admission was 12.three%, with a bacteremia rate of 29.9%, septic shock 11.4%, and mortality 0.38%. Just a few studies investigated the adventure factors for AKI in UTI patients. Previous studies indicated that hypovolemia, hypotension, sepsis, the utilize of nephrotoxic drugs, dissimilarity media and urinary obstruction were AKI risk factors in UTI patients [23, 24]. Our study showed that UTI patients with DM, upper UTI, afebrile or septic shock during hospitalization and impaired baseline renal function were at higher chance for development of AKI.

The take a chance of UTI in CKD patients might be increased by disease and host factors (e.one thousand., papillary necrosis, nephrolithiasis, neurogenic float, immunodeficiency, malnutrition, low urinary flow rate or urinary concentration defect) and management of comorbidity (foley catheters and intravenous lines) [25]. In addition, CKD has been recognized equally a risk cistron for development of AKI. A lot of comorbidities are associated with CKD, including loftier incidence of cardiovascular disease in CKD with increased exposure to contrast agents, use of ACE inhibitors or ARBs in the existence of undiagnosed renal artery stenosis, and impaired autoregulation of renal blood flow in diabetic patients permitting low renal perfusion during systemic hypotension. These comorbidities per se may lead to more frequent exposure to nephrotoxic agents and/or alter the response to an astute insult, which cause increased susceptibility to AKI [26]. Previous studies reported that CKD was a strong predictor of acute decline in kidney function following exposure to radio-dissimilarity and major surgery [27, 28]. Hsu et al. compared CKD patients with infirmary-acquired AKI treated with and without dialysis, and identified a significantly increased AKI risk if eGFR <60 mL/min/1.73 mii [29]. Moreover, subjects with eGFR of 45–59 mL/min/one.73 yard2 had on average a twofold increase in adjusted odds ratio of AKI compared with subjects with eGFR of 60 mL/min/1.73 k2 or above. In this written report, at that place was a higher incidence of eGFR of <60 mL/min/1.73 m2 in the AKI group compared with that in the non-AKI group (67.0% versus 32.9%, respectively). In improver, compared with subjects with baseline eGFR of sixty mL/min/one.73 m2 or to a higher place, the odds ratio for AKI in subjects with baseline eGFR 45–59 mL/min/1.73 mtwo, thirty–44 mL/min/1.73 chiliadii, and < thirty mL/min/1.73 m2 were ii.12, 4.44, and iv.72, respectively. Our results suggested that impaired baseline renal part played a predictive office for development of AKI in UTI patient.

Our report showed that the UTI patients with AKI were older than those without (72 ± thirteen versus 64 ± 19 years, P < 0.001), with an odds ratio of i.02 increase each year. UTI is a type of infection which is common amid older people. The prevalence of UTI in the elderly is much higher than younger individuals. At least 20% women and 10% of men aged 65 years or older have bacteriuria [30]. In our written report, 59.2% (468/790) of the cases are over 65 years erstwhile. Multiple age-related changes including prison cell-mediated amnesty recession, float defenses alteration due to obstructive uropathy, neurogenic dysfunction, bacterial receptivity intensification of uroepithelial cells [31], contamination due to fecal and urinary incontinence, uretheral instrumentation and catheterization, and antibacterial factors reduction in prostate and vagina associated with changes in zinc levels, PH and hormones [32] contribute to the take chances associated with UTI in elderly. Additionally, age-related turn down of GFR may crusade older patients at risk for acute kidney injury. [33] In our written report, patients who were over 65 years erstwhile had college prevalence of eGFR <60 compared with those nether 65 years old (53.ii% versus 13.7%, respectively). Since age and dumb baseline renal function are risks for development of AKI in UTI patients, physicians should pay attention to elderly UTI patients with CKD.

DM has been reported as a take chances gene for the development of both upper and lower UTIs [34–36]. In addition, DM is a potent predictor of AKI following exposure to contrast media [27], cardiac surgery [37, 38], oral sodium phosphate bowel preparation [39], and sepsis [40]. In our written report, UTI patients, compared with the full general population, had a higher incidence of DM (38.2%). In the AKI group, 56.7% had DM. Patients with diabetes had a college risk of AKI (OR 2.23, 95% CI 1.35–3.68, P = 0.002). UTI is one of the nigh common sources of bacteremia in diabetic patients [41], and patients with DM are at a greater risk of developing various complications of UTI including sepsis [42]. Severe sepsis may induce vital organ dysfunction, including AKI [43]. Robbins et al. showed that UTI induced acute kidney injury in approximately 40% of diabetic patients with bacteremia [44]. Our results also suggested that DM was an independent take a chance gene for AKI in UTI patients.

Fever is known as an important feature of sepsis, and is considered to be an adaptive response to strengthen the immune arrangement in order fighting confronting the invading organisms [45]. Lack of fever may contribute to lower resistance to infection, delayed recovery [17], higher mortality rate, and poor prognosis [46]. A number of factors, including astute alcoholism, hypothyroidism and elderliness have been identified in patients who had experienced afebrile bacteremia [47–49]. In this study, there was a college incidence of being afebrile in patients with AKI (59.8%) than those without AKI (44.nine%). Existence afebrile played a predictive role for AKI in UTI patient (OR one.71, 95% CI 1.04–ii.83, P = 0.036). Wolk PJ et al. found that patients with renal harm exhibited a lower febrile response to bacteremia [50]. Our study showed that 50.4% (137/272) of patients with eGFR <60 mL/min/1.73m2 experienced afebrile UTI. Amidst the UTI patients with eGFR <threescore mL/min/ane.73m2 developing AKI, 64.5% (40/62) presented with beingness afebrile. Several reasons might business relationship for afebrile UTI patients existence prone to developing AKI. First, patients with afebrile UTI accept higher chance to accept CKD, whereas CKD per se is a risk of AKI in UTI patients. Second, afebrile UTI with sepsis is more likely to be unrecognized, and more serious complications including AKI may result from the delayed treatment.

Upper UTI is not a well-recognized cause of AKI. Acute pyelonephritis can involve entire lobules of the medulla and cortex [51]. Interstitial infiltration of neutrophils and phagocytes and extensive destruction of the parenchymal by the acute inflammatory process were found in AKI patients with acute pyelonephritis [52. 53]. These reports demonstrated that severe upper UTI might cause serious damage to the kidney and resulted in AKI. Our study found that patients with upper UTI had higher take chances of AKI than those with lower UTI (OR two.63, 95% CI 1.53–4.56, P = 0.001). Early establishment of appropriate antibiotic therapy for patients with upper UTI, especially those with septic shock, is important to prevent the development of AKI.

It is well known that nephrotoxic medications contribute to the development of AKI [54, 55]. In this study, there was a lower incidence of AKI in patients treated with nephrotoxic agents compared with those not treated with nephrotoxic agents (8.7% versus 19.7%, respectively). Nephrotoxic agent was commonly avoided in patients with impaired baseline renal part, unstable hemodynamics, or at adventure of AKI. This would event in a lower incidence of use of nephrotoxic agents in patients developing AKI in this study.

There are several limitations in this study. Commencement, the retrospective data collection may pb to missing data and bias. Still, nosotros comprehensively collected the data using a standard form to reduce bias. 2d, although the treatments were prescribed by qualified attending physicians according to the standard treatment for UTI, medications potentially contribute to AKI (east.thou., aminoglycosides, nonsteroid anti-inflammatory drugs, dissimilarity media), which may issue in a potential bias. Nephrotoxic agents were usually avoided in patients with impaired baseline renal office or at take chances of AKI. Contrast media may be required for emergency imaging survey of complicated UTI, urosepsis, or septic stupor. Considering of the selection bias, putting the apply of nephrotoxic agent into the multivariate analysis will yield inaccurate results or conclusions. Further prospective studies will be needed to ostend the relationship between nephrotoxic agents and AKI in UTI patients. Third, this is a single middle study, and the results may not be generalized to the entire customs. A prospective, randomized written report with larger sample size volition exist needed to ostend our results. 4th, UTI patients' urine output was not routinely recorded in this retrospective study. Therefore, we could not use the definition of AKI based on the urine output of Kidney Disease: Improving Global Outcomes (KDIGO) criteria to define the development of AKI. Of course, this underestimated the true incidence of AKI in our UTI patients. A prospective study designed to record the serial serum creatinine and urine output subsequently admission will exist needed to provide the true incidence of AKI after UTI using the KDIGO criteria based on both serum creatinine and urine output criteria. In conclusion, we found that impaired baseline renal office, advancing age, DM, upper UTI, and afebrile during hospitalization are all of import and independent hazard factors for developing AKI in UTI patients. Physicians should pay attending to UTI patients at gamble of AKI.

Supporting Information

Author Contributions

Conceived and designed the experiments: MCW. Analyzed the data: CYH HYY MCH. Contributed reagents/materials/analysis tools: HYY PHH. Wrote the paper: CYH HYY MCH.

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    How Ckd Increases Risk For Utis,

    Source: https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0133835

    Posted by: daltonthisharm.blogspot.com

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