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作 者:邓婕 魏佳莉 DENG Jie;WEI Jiali(Department of Clinical Medicine,Hainan Medical University,Haikou 518110;Department of Nephrology,Hainan Hospital Affiliated to Hainan Medical University,Haikou 570311,China)
机构地区:[1]海南医科大学临床医学系,海南海口518110 [2]海南医科大学附属海南医院肾内科,海南海口570311
出 处:《基础医学与临床》2025年第3期378-381,共4页Basic and Clinical Medicine
基 金:国家自然科学基金(82160135)。
摘 要:高尿酸血症(HUA)导致尿酸(UA)代谢异常,尿酸盐在肾脏内蓄积,不仅影响肾小球滤过功能和肾小管重吸收功能,而且还引起氧化应激、炎性反应和上调肾素-血管紧张素-醛固酮系统(RASS)等机制损害肾脏细胞及组织,促进肾纤维化同时加速糖尿病肾病(DN,DKD)的发展。这些作用机制揭示了,HUA是DKD进展的危险因素,有效控制UA为延缓DKD发展有着重要作用。Hyperuricemia(HUA),characterized by abnormal uric acid(UA)metabolism,leads to the accumulation of urate salts within the kidney.This accumulation not only disrupts glomerular filtration and tubular reabsorption functions but also triggers oxidative stress,inflammation,and up-regulating the renin-angiotensin-aldosterone system(RASS),all of which damage renal cells and tissues.These mechanisms contribute to renal fibrosis and accelerate the progression of diabetic nephropathy(DN)/diabetic kidney disease(DKD).These findings underscore the role of HUA as a risk factor for the advancement of DKD,emphasizing the critical importance of effective UA control in delaying its development.
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