Infective endocarditis (IE) remains a dangerous disease and continues to have a high mortality rate. Unfortunately, despite continuous improvements in diagnostic methods, in many cases, blood cultures remain negative, and the pathogen causing endocarditis is unknown. This makes targeted therapy and the selection of appropriate antibiotics impossible. Therefore, we present what methods can be used to identify the pathogen in infective endocarditis. These are mainly molecular methods, including PCR and MGS, as well as imaging methods using radiotracers, which offer more possibilities for diagnosing IE. However, they are still not widely used in the diagnosis of IE. The article summarizes in which cases we should choose them and what we are most hopeful about in further research into the diagnosis of IE. In addition, registered clinical trials that are currently underway for the diagnosis of IE are also presented.

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.

One of the main causes of heart failure is cardiomyopathies. Among them, the most common is hypertrophic cardiomyopathy (HCM), characterized by thickening of the left ventricular muscle. This article focuses on HCM and other cardiomyopathies with myocardial hypertrophy, including Fabry disease, Pompe disease, and Danon disease. The genetics and pathogenesis of these diseases are described, as well as current and experimental treatment options, such as pharmacological intervention and the potential of gene therapies. Although genetic approaches are promising and have the potential to become the best treatments for these diseases, further research is needed to evaluate their efficacy and safety. This article describes current knowledge and advances in the treatment of the aforementioned cardiomyopathies.

Background: Protocol biopsies are performed to detect subclinical pathologies that may lead to future graft dysfunction. However, they are not routinely performed interventions in every transplant center. There is no established regimen for performing them. Purpose: The study aimed to evaluate if protocol biopsies can improve long-term patient outcomes after detecting early disorders and modifying treatment. Material and Methods Our observational study included 61 patients who underwent protocol biopsy 12 months after the transplantation. Based on the biopsy results, patients with abnormal histologic material (n = 37) were divided into 3 study groups as follows: patients with mild inflammatory lesions (n = 21), patients with interstitial fibrosis and tubular atrophy (IFTA) grade II to III (n = 12), and patients with BK virus nephropathy (n = 4). The control group (n = 24) included kidney recipients with IFTA 0 to I grade. Outcomes after 5-year follow-up were evaluated. Results: Five years after the biopsy, patients in the control group had stable graft function (5-year change in serum creatinine was -0.09 mg/dL). An increase in serum creatinine levels was observed in patients with IFTA II to III compared with the control group (0.14 mg/dL, P = .04). Immunosuppressive treatment was modified in the group with mild inflammatory changes and in the BKV group after the biopsy result. In the group with mild inflammatory lesions, renal function was stable (change of serum creatinine was -0.01 mg/dL, P = .51). In the BKV nephropathy group, there was a significant reduction in serum creatine levels (-0.48 mg/dL, P = .016). The analysis showed no diagnostic value for serum creatinine concentration (95% CI 0.49-0.78, P = .08). Conclusions: Protocol biopsies are useful for detecting early pathologies and preventing allograft failure. They greatly benefit patients with detectable pathology that can be treated or in whom therapy modification is possible.