Nanomedicine is currently showing great promise for new methods of diagnosing and treating many diseases, particularly in kidney disease and transplantation. The unique properties of nanoparticles arise from the diversity of size effects, used to design targeted nanoparticles for specific cells or tissues, taking renal clearance and tubular secretion mechanisms into account. The design of surface particles on nanoparticles offers a wide range of possibilities, among which antibodies play an important role. Nanoparticles find applications in encapsulated drug delivery systems containing immunosuppressants and other drugs, in imaging, gene therapies and many other branches of medicine. They have the potential to revolutionize kidney transplantation by reducing and preventing ischemia–reperfusion injury, more efficiently delivering drugs to the graft site while avoiding systemic effects, accurately localizing and visualising the diseased site and enabling continuous monitoring of graft function. So far, there are known nanoparticles with no toxic effects on human tissue, although further studies are still needed to confirm their safety.

Kidney transplantation (KTx) is the best treatment method for end-stage kidney disease. KTx improves the patient’s quality of life and prolongs their survival time; however, not all patients benefit fully from the transplantation procedure. For some patients, a problem is the premature loss of graft function due to immunological or non-immunological factors. Circulating cell-free DNA (cfDNA) is degraded deoxyribonucleic acid fragments that are released into the blood and other body fluids. Donor-derived cell-free DNA (dd-cfDNA) is cfDNA that is exogenous to the patient and comes from a transplanted organ. As opposed to an invasive biopsy, dd-cfDNA can be detected by a non-invasive analysis of a sample. The increase in dd-cfDNA concentration occurs even before the creatinine level starts rising, which may enable early diagnosis of transplant injury and adequate treatment to avoid premature graft loss. In this paper, we summarise the latest promising results related to cfDNA in transplant patients.

Gal-3, also known as galectin-3, a lectin that binds β-galactosides, has gained attention as a novel biomarker and pathophysiological mediator in cardiovascular disease, where it contributes to inflammation, fibrosis, metabolic dysregulation and cardiac remodeling. This narrative review, developed following SANRA (Scale for the Assessment of Narrative Review Articles) guidelines, aims to integrate current clinical and experimental findings on gal-3 into the American Heart Association Life’s Simple 7 (LS7) and Life’s Essential 8 (LE8). By thematically organizing our review across modifiable domains of cardiovascular health, including glucose regulation, lipid metabolism, physical activity, blood pressure, diet, sleep, tobacco use, and body weight (BMI, body mass index), we highlight the role of gal-3 in linking environmental, behavioral and molecular risk factors to cardiometabolic outcomes. Particular attention is given to the oxidative stress, inflammatory–fibrotic axis, and immune activation as mechanistic pathways underlying gal-3-associated cardiovascular damage. We also discuss its relevance to public health and prevention, considering gal-3’s potential for early risk stratification, monitoring lifestyle interventions and personalized prevention strategies. This review bridges molecular mechanisms with clinical and public health relevance, particularly in the context of environmental and lifestyle-related cardiovascular risk.

The dysregulation of both the innate and adaptive responses to SARS-CoV-2 have an impact on the course of COVID-19, and play a role in the clinical outcome of the disease. Here, we performed a comprehensive analysis of peripheral blood lymphocyte subpopulations in 82 patients with COVID-19, including 31 patients with a critical course of the disease. In COVID-19 patients who required hospitalization we analyzed T cell subsets, including Treg cells, as well as TCRα/β and γ/δ, NK cells, and B cells, during the first two weeks after admission to hospital due to the SARS-CoV-2 infection, with marked reductions in leukocytes subpopulations, especially in critically ill COVID-19 patients. We showed decreased levels of Th, Ts cells, Treg cells (both naïve and induced), TCRα/β and γ/δ cells, as well as CD16+CD56+NK cells in ICU compared to non-ICU COVID-19 patients. We observed impaired function of T and NK cells in critically ill COVID-19 patients with extremely low levels of secreted cytokines. We found that the IL-2/INFγ ratio was the strongest indicator of a critical course of COVID-19, and was associated with fatal outcomes. Our findings showed markedly impaired innate and adaptive responses in critically ill COVID-19 patients, and suggest that the immunosuppressive state in the case of a critical course of SARS-CoV-2 infection might reflect subsequent clinical deterioration and predict a fatal outcome.

Epicardial adipose tissue (EAT) exhibits morphological similarities with pericardial adipose tissue, however, it has different embryological origin and vascularization. EAT is a metabolically active organ and a major source of anti-inflammatory and proinflammatory adipokines, which have a significant impact on cardiac function and morphology. Moreover, it can regulate vascular tone by releasing various molecules. The relationship between EAT and cardiovascular disease and diseases of other organ systems is now considered a common discussion subject. The present clinical review article summarizes the epidemiological findings based on imaging techniques in studies conducted so far. In conclusion, evaluation of the epicardial adipose tissue constitutes a helpful scientific parameter, which can be assessed by means of different diagnostic imaging examinations.

Background/Objectives: Extracellular volume (ECV) of the myocardium, a biomarker of interstitial space and fibrosis, plays a critical role in cardiac disease diagnosis and prognosis. Although cardiac magnetic resonance imaging (MRI) is the gold standard for ECV assessment, computed tomography (CT) offers a viable alternative, particularly in patients with contraindications to MRI. This study aimed to assess whether CT-derived ECV is systematically elevated in cardiac diseases associated with myocardial fibrosis. Methods: A systematic search of PubMed and Web of Science up to January 2023 identified 364 studies, including 16 from registers and 4 from manual searches. After exclusions, 73 studies were included in the systematic review. Of these, 15 provided quantitative data on group sizes, mean ECV values, standard deviations, and imaging modalities (CTA, DECT, LIE-DECT) and were analyzed in the meta-analysis. Standardized mean differences (SMD) were calculated using Cochrane Handbook formulas. Statistical analyses employed random-effects models (R version 4.4.2). Results: The pooled analysis showed that ECV was significantly higher in pathological groups compared to controls (SMD 1.60; 95% CI: 1.23–1.96; I² = 84.6%). Elevated ECV correlated with worse clinical outcomes, including higher mortality in heart failure and advanced myocardial fibrosis in amyloidosis and cardiomyopathies. Subgroup analyses demonstrated that advanced CT techniques (DECT, LIE-DECT) and CTA provided comparable diagnostic accuracy. Conclusions: CT-derived ECV is a reliable, non-invasive marker of myocardial fibrosis, offering diagnostic and prognostic value similar to MRI. Standardizing CT protocols and conducting multicenter studies are essential to validate its broader clinical application.