高尿酸血症性肾病的发病机制及药物治疗
Pathogenesis and Treatment of Chronic Hyperuricemic Nephropathy

作者: 孟晓璐 , 杨宝学 , 周 虹 :北京大学医学部基础医学院药理学系,天然药物及仿生药物国家重点实验室,北京; 李 欣 :青岛大学附属医院,山东 青岛;

关键词: 痛风高尿酸血症慢性肾脏疾病药物治疗Gout Hyperuricemia Chronic Kidney Diseases (CKD) Medical Treatment

摘要:
近年来大规模流行病学研究发现,高尿酸血症与高血压、心脑血管疾病、糖尿病、代谢综合征等疾病的发生和发展密切相关,已成为威胁人类健康的严重代谢性疾病,也是肾脏疾病进展的独立危险因素。尿酸作为嘌呤代谢的终末产物,可以通过多种分子机制导致肾脏损伤,包括诱导炎症反应和肾脏间质纤维化,激活氧化应激,诱导肾小管上皮细胞向间质细胞转化(epithelial-to-mesenchymal transition, EMT)等。为了深入研究高尿酸血症性肾脏疾病的发病机制,寻找新的药物治疗靶点,本文对高尿酸血症性肾病发生发展的病理生理机制及其治疗药物的研究进展进行综述。

Abstract: Large numbers of epidemiological and clinical studies in recent years have accumulated that hyperuricemia may be strongly linked with many metabolic diseases, including hypertension, cardiac-cerebral vascular disease, diabetes and metabolic syndrome. It has been regarded as a severe disease threatening human health and an independent risk factor in the progression of kidney diseases as well. As the end product of purine metabolism, uric acid can induce renal injury through multiple mechanisms, such as inflammation, renal fibrosis, oxidative stress and epithelial-to-mesenchymal transition. To further study the pathogenesis of hyperuricemia nephropathy and potential targets involved, we mainly discuss the physiopathologic mechanism and medical treatment of hyperuricemia in this review.

文章引用: 孟晓璐 , 李 欣 , 杨宝学 , 周 虹 (2016) 高尿酸血症性肾病的发病机制及药物治疗。 生理学研究, 4, 1-9. doi: 10.12677/JPS.2016.41001

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