(1) Background: The interaction between the human body and the Earth’s magnetic field at Schumann resonances (SRs) is one of the important fundamental questions of science that continues to be studied. The aim of this study was to create a working theoretical foundation for the interaction of the human body with SRs. (2) Methods: Extensive research was carried out in the literature with the aim of comprehensively presenting data on SRs and creating a working concept of their interaction with the human body. (3) Results: General data on SRs, a theoretical basis for justifying their interaction with the human body, possible mechanisms of influence and research results on the functioning of human internal organs were presented. (4) An interaction of the human body with SRs exists and has been scientifically proven. This interaction has been studied most significantly between SRs and the human nervous system. SRs affect functional indicators of the cardiovascular system: heart rate and blood pressure. Studying the influence of SRs on the course and pathogenesis of non-communicable diseases is a promising direction. Low-frequency SRs decrease the risk of developing acute myocardial infarction, and there is a tendency for them to promote cases of chronic kidney disease. SRs are an important external natural factor influencing the human body.

Tacrolimus (TAC) has a narrow therapeutic window and patient-specific pharmacokinetic variability. In our study, we analyzed the association between TAC exposure, metabolism, and kidney graft outcomes (function, rejection, and histological lesions). TAC trough (C₀), coefficient of variation (TAC CV), concentration/dose ratio (C/D), and biomarkers related to kidney injury molecule-1 (KIM-1) and neutrophil gelatinase lipocalin (NGAL) were analyzed. We examined 174 patients who were subjected to a triple immunosuppressive regimen and underwent kidney transplantation between 2017 and 2022. Surveillance biopsies were performed at the time of kidney implantation and at three and twelve months after transplantation. We classified patients based on their Tac C/D ratios, classifying them as fast (C/D ratio < 1.05 ng/mL × 1/mg) or slow (C/D ratio ≥ 1.05 ng/mL × 1/mg) metabolizers. TAC exposure/metabolism did not significantly correlate with interstitial fibrosis/tubular atrophy (IF/TA) progression during the first year after kidney transplantation. TAC CV third tertile was associated with a higher chronicity score at one-year biopsy. TAC C/D ratio at three months and Tac C₀ at six months were associated with rejection during the first year after transplantation. A fast TAC metabolism at six months was associated with reduced kidney graft function one year (OR: 2.141, 95% CI: 1.044–4.389, p = 0.038) and two years after transplantation (OR: 4.654, 95% CI: 1.197–18.097, p = 0.026), and TAC CV was associated with reduced eGFR at three years. uNGAL correlated with IF/TA and chronicity scores at three months and negatively correlated with TAC C₀ and C/D at three months and one year. Conclusion: Calculating the C/D ratio at three and six months after transplantation may help to identify patients at risk of suffering acute rejection and deterioration of graft function.

Background/Objectives: This review has been prepared to promote interest in the interdisciplinary study of mitochondrial dysfunction (MD) and atherosclerosis. This review aims to describe the state of this problem and indicate the direction for further implementation of this knowledge in clinical medicine. Methods: Extensive research of the literature was implemented to elucidate the role of the molecular mechanisms of MD in the pathogenesis of atherosclerosis. Results: A view on the pathogenesis of atherosclerosis through the prism of knowledge about MD is presented. MD is the cause and primary mechanism of the onset and progression of atherosclerosis. It is proposed that this problem be considered in the context of a continuum. Conclusions: MD and atherosclerosis are united by common molecular mechanisms of pathogenesis. Knowledge of MD should be used to argue for a healthy lifestyle as the primary way to prevent atherosclerosis. The development of new approaches to diagnosing and treating MD in atherosclerosis is an urgent task and challenge for modern science.

Background/Objectives: Noncommunicable diseases (NCDs) are a very important medical problem. The key role of mitochondrial dysfunction (MD) in the occurrence and progression of NCDs has been proven. However, the etiology and pathogenesis of MD itself in many NCDs has not yet been clarified, which makes it one of the most serious medical problems in the modern world, according to many scientists. Methods: An extensive research in the literature was implemented in order to elucidate the role of MD and NCDs’ risk factors in the pathogenesis of NCDs. Results: The authors propose to take a broader look at the problem of the pathogenesis of NCDs. It is important to understand exactly how NCD risk factors lead to MD. The review is structured in such a way as to answer this question. Based on a systematic analysis of scientific data, a theoretical concept of modern views on the occurrence of MD under the influence of risk factors for the occurrence of NCDs is presented. This was done in order to update MD issues in clinical medicine. MD and NCDs progress throughout a patient’s life. Based on this, the review raised the question of the existence of an NCDs continuum. Conclusions: MD is a universal mechanism that causes organ dysfunction and comorbidity of NCDs. Prevention of MD involves diagnosing and eliminating the factors that cause it. Mitochondria are an important therapeutic target.

With an increasing number of marginal donors, additional methods for the evaluation of cadaveric kidney quality are required. This study aimed to evaluate pretransplant deceased donor serum (s) and urine (u) biomarkers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-18, and C-X-C motif chemokine 10 (CXCL10) for predicting early and late graft function. In total, 43 deceased kidney donors and 76 corresponding recipients were enrolled. Delayed graft function (DGF) occurred in 27.6% of cases. sIL-18, sKIM-1, uNGAL, and uKIM-1 were predictors of DGF. A model incorporating sIL-18, uKIM-1, and clinical factors was developed to predict DGF (AUROC 0.863). Univariate analysis showed a negative association between uKIM and graft eGFR at 6, 12, 24, and 36 months, but this was not confirmed in the multivariate analysis. In conclusion, we report a superior performance of donor biomarkers for predicting DGF and later graft function over serum creatinine. Higher levels of donor sIL-18 and uKIM in conjunction with expanded-criteria donors and longer cold ischemia times predicted DGF. With no renal tubular damage in zero-time donor biopsies, higher pretransplant urine and serum NGAL levels were associated with better allograft function one year after transplantation, and sNGAL with graft function three years after transplantation.

The objective of the present study was to compare principal cell-specific aquaporin-2 (AQP2) abundances in urinary extracellular vesicles (uEVs) on the first postoperative day in deceased-donor kidney transplant recipients without and with acute kidney injury. We measured uEV markers (CD9 and CD63) and the abundances of proximal tubular sodium-glucose transporter 2, distal tubular sodium/chloride cotransporter, and principal cell-specific aquaporin-2 using Western blotting of urine. uEV-AQP2 levels were normalized to living donor controls. The validation cohort consisted of 82 deceased-donor kidney transplant recipients who had a median age of 50 years (IQR 43 to 57 years). A total of 32% of recipients had acute kidney injury. The median uEV-AQP2 was significantly higher in recipients with acute kidney injury compared to immediate allograft function (2.05; IQR 0.87 to 2.83; vs. 0.81; IQR 0.44 to 1.78; p < 0.01). The Youden index indicated a uEV-AQP2 threshold of 2.00. Stratifying uEV-AQP2 into quartiles showed that recipients with higher uEV-AQP2 levels had higher rates of acute kidney injury (Cochran–Armitage, p = 0.001). The discovery cohort showed elevated CD9, CD63, and uEV-AQP2 levels in urine from recipients with acute kidney injury compared to immediate allograft function. We were able to quantify the damage of principal cells after kidney transplant to predict acute kidney injury using uEV-AQP2.