CELLULAR AND MOLECULAR MECHANISMS OF KIDNEY TISSUE DAMAGE IN HYPERURICEMIA
Keywords:
Hyperuricemia, Kidney Injury, Oxidative Stress, Inflammation, Apoptosis, Fibrosis.Abstract
Hyperuricemia, defined by elevated blood uric acid levels, is a common metabolic disorder that can lead to kidney dysfunction in addition to gout. Excess uric acid induces cellular and molecular changes in renal tissue, including oxidative stress, inflammation, apoptosis, and fibrosis. Both urate crystal-dependent and crystal-independent mechanisms contribute to renal injury, affecting endothelial function, tubular epithelial cells, and interstitial fibroblasts. Understanding these cellular and molecular pathways is crucial for developing early diagnostic, preventive, and therapeutic strategies. This paper reviews the current knowledge of the mechanisms underlying hyperuricemia-induced kidney damage, highlighting potential targets for treatment and improved patient outcomes.
References
1. Su, H.-Y., Zhang, H., & Sun, L. (2020). Research advances in the mechanisms of hyperuricemia-induced renal injury: Oxidative stress, inflammation, endothelial dysfunction and fibrosis. PubMed, 14(3), 112–128.
2. Азимова, А. А., Маликов, Д. И., & Шайкулов, Х. Ш. (2021). МОНИТИРОИНГ ЭТИОЛОГИЧЕСКОЙ СТРУКТУРЫ СЕПСИСА ЗА. PEDAGOGICAL SCIENCES AND TEACHING METHODS, 48, 18-22.
3. Luo, Y., Song, Q., Li, J., et al. (2024). Effects of uric acid-lowering therapy on renal outcomes in CKD patients with asymptomatic hyperuricemia: Systematic review and meta-analysis. BMC Nephrology, 25, 112–127.
4. Kanbay, M., Segal, M., Afsar, B., et al. (2016). The role of uric acid in the pathogenesis of renal disease. Journal of the American Society of Nephrology, 27, 37–45.
5. АЗИМОВА, А. А., & МАЛИКОВ, Д. И. (2022). ПОВРЕЖДЕНИИ МЯГКОТКАНЫХ СТРУКТУР КОЛЕННОГО СУСТАВА И УЛЬТРАЗВУКОВОЕ ИССЛЕДОВАНИЕ. МОЛОДЕЖНЫЙ ИННОВАЦИОННЫЙ ВЕСТНИК Учредители: Воронежский государственный медицинский университет имени НН Бурденко, 11(2), 10-13.
