Background: Urinary tract infections (UTIs) are the most common bacterial infections among kidney transplant (KTX) recipients. The purpose of this study was to analyze antimicrobial resistance (AMR) in four most common pathogens responsible for UTIs in KTX recipients and determine risk factors (RF) for resistance in the same group. Methods: Analyzed antibiograms were based on urine samples positive for bacterial growth of 105 colony-forming units (CFU)/mL obtained from hospitalized adult KTX recipients presenting with UTI symptoms upon admission to the center in years 2011–2018. Results: In total, 783 antibiograms were analyzed for Klebsiella pneumoniae (258 samples, 33.0%), Escherichia coli (212, 27.0%), Enterococcus faecalis (128, 24.0%), and Enterococcus faecium (125, 16.0%). The decrease in susceptibility of E. coli to amoxicillin/clavulanic acid (62.9% vs. 40.0%) and ciprofloxacin (100% to 40.0%) was observed. Susceptibility to gentamicin increased from 33.3% to 92.9% in E. faecium. Susceptibility to tigecycline remained 100% through all years in case of E. faecalis and E. faecium. Male gender was a RF for resistance to amoxicillin/clavulanic acid (p = 0.008), ciprofloxacin (p = 0.0003), trimethoprim/sulfamethoxazole (p = 0.00009), ceftriaxone (p = 0.0001), and cefuroxime axetil (p = 0.00038) in K. pneumoniae and against gentamicin in E. faecalis (p = 0.015). Higher resistance to ampicillin in E. faecalis (p = 0.012) and to ciprofloxacin (p = 0.0003), trimethoprim/sulfamethoxazole (p = 0.007), piperacillin/tazobactam (p = 0.003), ceftriaxone (p = 0.001), and cefuroxime axetil (p = 0.013) in K. pneumoniae was observed in higher age groups of patients. Diabetes as a cause of kidney insufficiency (p = 0.026) and kidney-pancreas transplantation (p = 0.014) was RF for resistance to ceftriaxone in K. pneumoniae. Conclusions: AMR in uropathogens from KTX recipients fluctuated. There were identifiable RFs for resistance in the examined bacteria–antibiotic combinations. We recommend continuous mapping of site-specific microorganisms as etiology and susceptibility may vary between institutions and over time.

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Background: Chemokines (chemotactic cytokines) are small proteins which are engaged in many pathophysiological processes, including inflammation and homeostasis. In recent years, application of chemokines in transplant medicine was intensively studied. The aim of this study was to determine the utility of urinary chemokines CCL2 (C-C motif ligand 2) and CXCL10 (C-X-C motif chemokine ligand 10) in prognosis of 5-year graft failure and mortality post 1-year protocol biopsy in renal transplant recipients.Methods: Forty patients who had a protocol biopsy 1 year after renal transplantation were included. Concentrations of CCL2 and CXCL10 in urine with reference to urine creatinine were measured. All patients were under the supervision of one transplant center. Long-term outcomes within 5 years after 1-year posttransplant biopsy were analyzed.Results: Urinary CCL2:Cr at the time of biopsy was significantly increased in patients who died or had graft failure. CCL2:Cr was proven to be a significant predictor of 5-year graft failure and mortality (odds ratio [OR]: 1.09, 95% confidence interval [CI]: 1.02-1.19, p = .02; OR: 1.08, 95% CI: 1.02-1.16, p = .04; respectively). Conclusion:Chemokines are easily detected by current methods. In the era of personalized medicine, urinary CCL2:Cr can be considered as a factor providing complementary information regarding risk of graft failure or increased mortality.

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Patients with abdominal aortic aneurysm (AAA) have a higher risk of cardiovascular (CV) events, which seems to be associated with disturbed platelet (PLT) function. Endovascular aneurysm repair (EVAR) is an emerging, less-invasive treatment alternative to surgical AAA repair. Both platelet function abnormalities in patients with AAA and the effect of EVAR on platelet function are poorly understood. In this review, we aim to fill the gap regarding the effect of EVAR on PLT function in AAA patients by discussing PLT function disturbances in patients with AAA, PLT function changes after EVAR, evidence from clinical studies regarding PLT function before and after EVAR, and antiplatelet or and antithrombotic treatment in patients undergoing EVAR. The goal of our review is to summarize the contemporary knowledge and initiate further studies to better understand PLT function changes in patients undergoing EVAR, optimize the pharmacotherapy before and after EVAR and further improve outcomes in this group of patients.