Vol 17, No 2 (2025)

Objective. Evaluation of the gender features of the severity of hematuria that occurs during spontaneous elimination of stones from the urinary tract, and to identify receptors that modulate intracellular signaling during the development of compensatory mechanisms of platelet aggregation in women and men.

Material and methods. The study included 89 women (Group 1) and 61 men (Group 2) with nephrolithiasis, in whom hematuria was detected during examination. The activity of receptors regulating proaggregant activity of platelets was analyzed, in particular, purine P2Y-, PX1-receptors, TR-receptor, α₂-adrenoreceptor, GPVI-receptor, PAF-receptor, and adenosine A2A-receptor; agonists in concentrations EC50, causing aggregation at the level of 50% in healthy individuals, were used. Modeling of synergism of signaling pathways was reproduced by incubating platelets with subthreshold concentrations of agonists (EC10). Platelet aggregation was assessed by turbidimetric method on the ChronoLog analyzer (USA). Statistical analysis was performed using the MedCalc package.

Results. In the 1st group, severe hematuria (62,0±1,9 RBC per field) developed against the background of hyperreactivity of the PAF receptor and TR receptor, normoreactivity of the α₂-adrenoreceptor, purine P2X1 receptor, P2Y receptors, hyporeactivity of the adenosine A2 receptor and GPVI receptor. In the 2nd group, moderate microhematuria (35,9±1,9 RBC per field) was caused by hyperreactivity of the PAF receptor and TR receptor, normoreactivity of purine P2Y receptors, P2X1 receptor, adenosine A2 receptor and GPVI receptor, as well as hyporeactivity of the α₂-adrenoreceptor. Limitation of hematuria in the 1st group was ensured by the synergism of the PAF receptor, TR receptor and α₂-adrenoreceptor, in the 2nd group - PAF receptor, TR receptor and P2Y receptors. Optimal aggregation parameters in women were achieved through the interaction of signaling pathways associated with Gq and G12/13 (TR receptor) and Gi (α₂-adrenoreceptor) proteins; in men - with co-activation of signaling pathways associated with Gq, G12/13 (TR receptor) and Gq, Gi (P2Y receptors) proteins.

Conclusion. Further understanding of the mechanisms of intracellular platelet signaling associated with the GPCR receptor system will optimize the tactics of drug therapy for hematuria associated with nephrolithiasis.

Background. Chronic kidney disease (CKD) is a widespread chronic non-infectious disease that represents a serious medical and social problem. One of the early laboratory manifestations of CKD is anemia, the incidence of which increases as renal dysfunction progresses. Nephrogenic anemia is considered as a factor contributing to the progression of CKD and the development of its complications.

Objective. Assessment of the prevalence of anemia and its relationship with renal function parameters in patients with CKD.

Material and methods. The study included 887 patients with CKD of various etiologies, including 419 men (mean age 47,5 years) and 468 women (mean age 52,4 years). All patients underwent a comprehensive clinical and laboratory examination with an assessment of red blood parameters and renal filtration rates.

Results. Anemia was detected in 50,2% of patients with CKD at the pre- and predialysis stages. Its prevalence among women (51,9%) was slightly higher than among men (48,4%). The average levels of hemoglobin (Hb) and hematocrit (Ht) in men (125,5 g/L and 41,8%, respectively) were significantly higher than in women (111,7 g/L and 38,9%; p<0,05). Hypercholesterolemia was diagnosed more often in women (43,8%) than in men (36,0%). In men with CKD, a significant inverse correlation between the Hb (r=-0,542; p<0,001) and Ht (r=-0,547; p<0,001) concentration with the glomerular filtration rate (GFR), as well as the blood non-protein nitrogen (r=-0,434; p<0,005) and blood urea (r=-0,462; p<0,001) levels was found. In women, the Hb concentration also correlated with the GFR (r=-0.477; p<0.005), blood non-protein nitrogen (r=-0.525; p<0.001) and blood urea level (r=-0,528; p<0,001). In addition, a weak but statistically significant correlation of Hb concentration with total cholesterol level was found in women (r=-0,130; p<0,05), and the red blood cell count correlated with total cholesterol level (r=-0,118; p<0,05).

Conclusion. Anemia occurs in 50.2% of patients with CKD and is an important predictor of chronic renal failure progression, especially in women.

Objective. Evaluation of the dynamics of blood serum markers of fibroplastic transformation of the kidney in unilateral ureteral obstruction.

Material and methods. The study was approved by the local ethics committee of Yaroslavl State Medical University. A prospective comparative study was conducted, which included 33 patients with urolithiasis and unilateral ureteral obstruction caused by a stone less than 7 mm, and 15 healthy volunteers. The concentration of profibrotic cytokines TGF-β1 and CTGF was determined by ELISA. Diagnostics was performed using ultrasound and plain urography.

Results. In patients with ureteral obstruction, serum TGF-β1 (264±16.9 ng/ml) and CTGF (1141±33.1 ng/ml) concentrations at admission were significantly higher (p<0.001) than in the control group (TGF-β1 – 33±6.9 ng/ml, CTGF – 216.3±56.9 ng/ml). After 1 week, a sharp increase in TGF-β1 (18,239±556 ng/ml) and CTGF (45,765±123 ng/ml) levels was observed, indicating the development of severe fibrosis. After 1 month, blood cytokine concentrations decreased but remained above control values. Complete normalization of TGF-β1 (45±5.2 ng/ml) and CTGF (177±11.9 ng/ml) levels was observed only 2 months after obstruction elimination. In patients with prolonged obstruction (3–7 days), cytokine levels were significantly higher (p=0.03), indicating more pronounced fibrosis formation.

Conclusion. Unilateral ureteral obstruction leads to a significant increase in plasma TGF-β1 and CTGF levels, indicating the development of renal tissue fibrosis. The duration of obstruction affects the degree of fibrosis, emphasizing the need for early intervention and the promise of antifibrotic therapy.

Background. Fabry disease (FD) is a hereditary disorder caused by a decrease or complete absence of the α-galactosidase enzyme. It is characterized by a variety of clinical manifestations, which makes its diagnosis difficult.

Objective. Demonstration of clinical «masks» of Fabry disease using the case history of patient M.

Description of the clinical case. Patient M., 32 years old. Since the age of 7, he had noted acroparesthesia, hypohidrosis, periodic subfebrile temperature, lymphadenopathy, and later the appearance of proteinuria. Rheumatoid arthritis and systemic lupus erythematosus were suggested; methotrexate and methylprednisolone were prescribed – without effect. Based on the results of a nephrobiopsy, Fabry disease was suspected. The diagnosis was confirmed by molecular genetic and biochemical studies. Agalsidase α was prescribed, against this background, the severity of symptoms decreased.

Conclusion. Fabry disease is a rare disease that is difficult to diagnose. Renal biopsy is not the primary diagnostic method for Fabry disease, but in this case it was crucial for its verification, which provided adequate therapy and improvement of the patient’s condition.

Vascular access to the forearm in patients undergoing systemic hemodialysis (HD) is one of the key conditions for adequate HD. In situations where it is impossible to create vascular access in the upper limbs and there is total stenosis of the central veins, it is necessary to consider alternative vascular access routes. Formation of femoral arteriovenous fistula (AVF) is one of the possible places for creating such access. The article describes a rather rare type of vascular access, namely, transposition of the vena saphena magna in the form of a linear AVF with anastomosis of the femoral artery in the lower third. The course of the operation is described.

A search in MEDLINE/PubMed, EMBASE, Web of Science and Elibrary.ru databases using the keywords: paraneoplastic glomerulopathy, indolent lymphomas was conducted in order to study various variants of kidney damage in lymphoproliferative diseases (LPD). Kidney damage can be diagnosed at the onset of LPD or during its progression, relapse. At the same time, it is possible to verify the presence of LPD based on the results of a nephrobiopsy in the absence of a characteristic clinical picture of a hematological disease. The causes of kidney damage in oncohematological practice include specific lymphoid infiltration of the organ, aggravation of comorbid pathology, additional infection, paraneoplastic reactions, tumor lysis syndrome and toxic kidney damage by drugs with damage to the glomeruli, tubules or vessels of the kidneys.

The article examines the issue of legal regulation of off-label drug prescriptions to adult patients.

The author analyzed current legislative documents regulating the use of off-label drugs. Shortcomings in the legal framework including the lack of a unified procedure regulating the use of drugs outside the instructions in adults were identified. The identified uncertainty in the procedures for prescribing such drugs emphasizes the need to improve the regulatory system. The legislation regarding the prescription of drugs outside the instructions to children is analyzed. The role of medical commissions in making decisions on prescribing off-label therapy is considered. The need for a unified assessment of the actions of healthcare workers who prescribe drugs outside the instructions to adult patients in the context of the growth of new, poorly studied diseases is emphasized. The judicial practice on disputes related to off-label drug prescriptions to patients was also studied, including civil and criminal liability measures applied to doctors and medical organizations.

Based on the results of the analysis, author made a conclusion about the possibility of extending the procedures in force for off-label drug prescriptions to children to the adult population, as well as creating flexible adaptive legal solutions for the use of such drugs before their official inclusion in clinical guidelines, which will help minimize legal risks for healthcare workers and provide patients with access to the novel therapeutic approaches.

Early identification of kidney disease can protect kidney health, prevent kidney disease progression and related complications, reduce cardiovascular disease risk and decrease mortality. We must ask “Are your kidneys ok?” using serum creatinine to estimate kidney function and urine albumin to assess for kidney and endothelial damage. Evaluation for causes and risk factors for chronic kidney disease (CKD) includes testing for diabetes and measurement of blood pressure and body mass index. This World Kidney Day we assert that case-finding in high-risk populations, or even population level screening, can decrease the burden of kidney disease globally. Early-stage CKD is asymptomatic, simple to test for and recent paradigm shifting CKD treatments such as sodium glucose co-transporter-2 inhibitors dramatically improve outcomes and favor the cost-benefit analysis for screening or case-finding programs. Despite this, numerous barriers exist, including resource allocation, healthcare funding, healthcare infrastructure and healthcare-professional and population awareness of kidney disease. Coordinated efforts by major kidney non-governmental organizations to prioritise the kidney health agenda for governments and aligning early detection efforts with other current programs will maximise efficiencies.