CELLULAR AND MOLECULAR MECHANISMS OF KIDNEY TISSUE DAMAGE IN HYPERURICEMIA
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.