Pathogenesis and Treatment of Chronic Hyperuricemic Nephropathy

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。 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 syndrome. It has been regarded as a severe disease threatening human health an independent risk factor the progression kidney diseases well. As end product purine metabolism, uric acid can induce renal injury through multiple mechanisms, such inflammation, fibrosis, oxidative stress epithelial-to-mesenchymal transition. To further study pathogenesis nephropathy potential targets involved, we mainly discuss physiopathologic mechanism medical treatment this review.