Please use this identifier to cite or link to this item: http://repo.tma.uz/xmlui/handle/1/4409
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dc.date.accessioned2026-06-15T08:20:28Z-
dc.date.available2026-06-15T08:20:28Z-
dc.date.issued2026-
dc.identifier.urihttp://repo.tma.uz/xmlui/handle/1/4409-
dc.description.abstractIntroduction. Chronic kidney disease (CKD) is a global health priority due to its high prevalence (9-12% of the adult population), relentless progression, and early disability. The progression of CKD to end-stage renal disease (CKD stage 5) involves a complex interplay of hemodynamic, inflammatory, and metabolic factors. Key pathogenetic mechanisms include disturbances in nutritional status (protein-energy wasting, sarcopenia), an imbalance in the matrix metalloproteinase (MMP) system leading to renal fibrosis, and genetically determined features of the renin-angiotensin-aldosterone system (RAAS). Despite current treatment standards, CKD progression rates remain high, highlighting the need for an integrated, personalized approach combining nutritional, molecular, and genetic markers. Objective: To study the characteristics of nutritional status and matrix metalloproteinase levels in CKD, evaluate their role in the development of end-stage renal disease, and based on the findings, develop methods for the correction and prevention of disease progression. The study included 576 CKD patients observed in a nephrology hospital from 2021 to 2023. The study design was combined (retrospective and prospective). The retrospective group consisted of 423 patients for clinical course analysis. The prospective group included 153 patients who underwent in-depth examination. Methods included: clinical-anamnestic, anthropometric (BMI, waist circumference), nutritional status assessment using the Subjective Global Assessment (SGA) scale, instrumental methods (Doppler ultrasound of renal arteries with resistance index RI calculation, bioimpedance analysis), laboratory methods (eGFR, proteinuria, ferritin, vitamins B6, D, and folic acid), and molecular-genetic methods (genotyping of AGTR1 A1166C and AGTR2 G1675A polymorphisms, measurement of MMP-2 and MMP-9 levels). Statistical analysis included parametric and non-parametric methods, logistic regression, and ROC analysis.en_US
dc.language.isoen_USen_US
dc.titleASSESSMENT OF THE CLINICAL AND PATHOGENETIC MECHANISMS UNDERLYING THE PROGRESSION OF CHRONIC KIDNEY DISEASE AND METHODS FOR THEIR CORRECTIONen_US
dc.typeArticleen_US
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