Vol 98, No 6 (2026): Issues of nephrology

Autoantibody-producing B cells, as well as T cells, neutrophils, and macrophages, play a key role in the pathogenesis of immune-mediated glomerulopathies. Traditional therapy of glomerulonephritis (CGN) with corticosteroids or combination of corticosteroids with immunosuppressants is associated with serious adverse events and often with the therapy resistance. Recently B cell depletion, modulation of T cell differentiation have become a promising areas in the CGN treatment. Genetically modified T cells with chimeric antigenic receptors (CAR) or with chimeric antibodies receptors (CAAR) are capable to destroy effector B cells, as well as to reduce the production of autoantibodies responsible for glomerular damage. CAR-based strategies may give a better chance for more deep and durable CGN remission than the traditional and recently approved methods of pathogenic therapy of CGN. Promising data from preclinical studies suggest that CAR/CAAR-T therapy may be an important step towards remissions of resistant CGN. Clinical studies are needed to evaluate the long-term effectiveness and safety of this immunotherapy for patients with CGN.

Aim. To investigate the relationship between vitamin D levels, metabolic-associated fatty liver disease (MAFLD), and arterial stiffness.

Materials and methods. This study included 303 patients with a median age of 55 [40; 65] years. All participants underwent duplex ultrasonography with assessment of carotid extra-media thickness (EMT), and liver transient elastography with evaluation of the attenuation coefficient (AC) transthoracic echocardiography for measurement of epicardial adipose tissue thickness (EAT). MAFLD was diagnosed based on hepatic steatosis combined with overweight/obesity and at least two metabolic risk factors. Arterial stiffness was evaluated using the cardio-ankle vascular index (CAVI), measured by sphygmomanometry with the VaSera-1000 system FUCUDA DENSHI (Japan). Serum 25-hydroxyvitamin D levels were measured in all participants. Statistical analysis was performed using Statistica 12.0 software.

Results. Patients were divided into 4 groups depending on their vitamin D levels. High arterial stiffness was significantly more frequent in patients with severe vitamin D deficiency compared with those with insufficiency and optimal levels (40% vs 19.5%; p=0.006; 40% vs 0%; p<0.0001 respectively). The cardio-ankle vascular index (CAVI) was significantly higher in the severe deficiency group compared with the optimal vitamin D group (7.5 [6.5; 8.8] vs 6.6 [5.8; 7.5]; p=0.03). Significant correlations were observed between CAVI and EMT, EAT, AC, and the presence of MAFLD. Vitamin D levels were negatively correlated with AC and MAFLD. ROC analysis demonstrated the highest diagnostic accuracy for detecting increased arterial stiffness using a combined model (AUC _{vit D + AC + EMT} =0.823; p<0.0001).

Conclusion. Vitamin D is associated with arterial stiffness and ectopic fat deposition, while its combination with AC and EMT provides high diagnostic accuracy for identifying patients at increased cardiometabolic risk.

Background. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired, life-threatening disease of the blood characterized by intravascular hemolysis by the complement system, thrombotic events and bone marrow failure. The introduction of the C5 complement inhibitor eculizumab into clinical practice has presented new opportunities for the treatment of PNH and its complications, increasing patient survival and quality of life. However, clinically significant variability in treatment response is observed. One of the reasons is patients’ poor treatment adherence (TA), which is associated with a number of factors, including insufficient doctor attention to this problem and inconsistent eculizumab availability in some regions.

Aim. To evaluate the impact of eculizumab TA on the attainment of favorable clinical outcomes in patients with PNH in actual clinical practice.

Materials and methods. A review of published literature and our own data regarding the use of eculizumab for the treatment of PNH has been conducted.

Results. Long-term management of chronic conditions requires adequate adherence to treatment plans in order to achieve effective results. One of the key factors that can influence adherence is the doctor's lack of activity. To achieve PNH treatment goals, it is essential to consider predictors of appropriate / inappropriate adherence. An analysis of the outcomes of eculizumab treatment for PNH patients in Moscow City Hematology Center of Botkin Moscow Multidisciplinary Scientific and Clinical Center revealed that monitoring the frequency of infusions led to a 21% improvement in the optimal response rate to eculizumab therapy, compared to the outcomes of previous pathogenic treatment administered in regional centers.

Conclusion. Eculizumab has proven its efficacy and good tolerability and is widely used as a pathogenetic therapy for PNH. It is essential to strictly adhere to the eculizumab treatment regimen in order to achieve optimal results. It is essential for healthcare professionals to closely monitor patient motivation to adhere to their treatment plan. Effective communication between the healthcare provider and the patient is essential for the successful use of eculizumab. It is essential for specialists to make every effort possible to improve patient AT.

Pulmonary hypertension (PH) and chronic kidney disease (CKD) represent a complex combination that requires an interdisciplinary approach to the diagnosis and treatment of this category of patients. PH is both the cause and the result of the progression of CKD. Various studies have demonstrated the impact of PH on clinical outcomes in patients with CKD and kidney failure. The multifactorial pathogenesis of PH in patients with CKD has not been sufficiently studied to date. An important part of the pathogenesis is the development of endothelial dysfunction. The large randomized clinical trials and the clinical guidelines for the treatment of PH in patients with CKD or kidney failure are currently lacking.

To date, the role of various types of programmed cell death in the occurrence and progression of infectious diseases has been established. One such type, ferroptosis, which was recently discovered, is characterized by iron-dependent lipid peroxidation and is under investigation in relation to the development of disorders of various organ systems, including infections. Recent researches have revealed previously unknown mechanisms of bacterial damage associated with ferroptotic cell death. For instance, the involvement of ferroptosis in infections caused by multidrug-resistant pathogens such as Pseudomonas aeruginosa, Mycobacterium tuberculosis, Klebsiella pneumonia, and Escherichia coli has been demonstrated. The studied pathogenic mechanisms of these pathogens highlight ferroptosis as a potential therapeutic target for infectious diseases and suggest new possibilities for addressing the challenging problem of antibiotic resistance. In this review, we have summarized the main mechanisms of ferroptosis and highlighted new data on the pathogenic aspects of bacterial damage associated with this process. This information may be useful for developing new therapeutic strategies to combat this condition.