INFLUENCE OF URIC ACID ON RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM ACTIVITY IN CHRONIC KIDNEY DISEASE

Hyperuricemia plays a significant role in the progression of chronic kidney disease by modulating the activity of the renin-angiotensin-aldosterone system. Elevated uric acid levels promote oxidative stress, endothelial dysfunction, and inflammation, which contribute to increased renin, angiotensin II, and aldosterone production. These hormonal changes lead to vasoconstriction, sodium and water retention, hypertension, and renal fibrosis, accelerating kidney injury. Clinical and experimental evidence suggests that early management of hyperuricemia, combined with interventions targeting the renin-angiotensin-aldosterone system, can slow disease progression, reduce proteinuria, and improve patient outcomes. Understanding the interplay between uric acid and hormonal regulation is essential for developing effective therapeutic strategies in patients with chronic kidney disease.高尿酸血症（Hyperuricemia）通过调节肾素-血管紧张素-醛固酮系统（renin-angiotensin-aldosterone system）的活性，在慢性肾脏病（chronic kidney disease）的病程进展中扮演关键角色。血尿酸水平升高可诱发氧化应激、内皮功能障碍与炎症反应，进而促进肾素、血管紧张素II及醛固酮的合成与分泌增加。上述激素水平的异常改变会引发血管收缩、水钠潴留、高血压及肾纤维化，加速肾脏损伤进程。现有临床与实验证据显示，对高尿酸血症进行早期干预，并联合针对肾素-血管紧张素-醛固酮系统的治疗措施，能够延缓疾病进展、减少蛋白尿，并改善患者的临床结局。明确血尿酸与激素调控之间的相互作用机制，对于开发慢性肾脏病患者的有效治疗方案具有重要意义。