Li Kaiqing, Xia Xue, Fu Tong, Ma Yanchun, Wang Yingwei, Fan Mingming, Wang Songyan, Xing Guoli, Tong Ying
Heilongjiang University of Chinese Medicine, Harbin, China.
Brandeis University, Waltham, China.
Medicine (Baltimore). 2024 Dec 20;103(51):e40975. doi: 10.1097/MD.0000000000040975.
Hyperuricemic nephropathy is a metabolic disease in which renal uric acid deposition and excretion are impaired due to elevated levels of uric acid in the blood, leading to impaired renal tubule function and chronic renal disease. Hyperuricemic nephropathy is one of the important complications of hyperuricemia, which seriously affects the quality of life and prognosis of patients. The pathogenesis of hyperuricemic nephropathy involves a variety of factors, including: amino acid metabolism disorder, energy metabolism abnormality, increased nucleotide metabolism, lipid metabolism disorder and bile acid metabolism imbalance, REDOX process disorder, cell cycle and apoptosis imbalance, signal transduction and inflammatory response enhancement, and intestinal flora imbalance. In recent years, omics techniques such as metabolomics, transcriptomics and intestinal microecology have been used to reveal the metabolic, gene and microflora characteristics of hyperuricemic nephropathy from different levels, as well as their interactions and regulatory mechanisms. This paper reviews these studies, analyzes the existing problems and challenges, and puts forward future research directions and suggestions, aiming at providing new theoretical basis and practical guidance for the prevention and treatment of hyperuricemic nephropathy.
高尿酸血症肾病是一种代谢性疾病，由于血液中尿酸水平升高，导致肾脏尿酸沉积和排泄受损，进而引起肾小管功能障碍和慢性肾病。高尿酸血症肾病是高尿酸血症的重要并发症之一，严重影响患者的生活质量和预后。高尿酸血症肾病的发病机制涉及多种因素，包括：氨基酸代谢紊乱、能量代谢异常、核苷酸代谢增加、脂质代谢紊乱和胆汁酸代谢失衡、氧化还原过程紊乱、细胞周期和细胞凋亡失衡、信号转导和炎症反应增强以及肠道菌群失衡。近年来，代谢组学、转录组学和肠道微生态学等组学技术已被用于从不同层面揭示高尿酸血症肾病的代谢、基因和微生物群落特征，以及它们之间的相互作用和调控机制。本文对这些研究进行综述，分析存在的问题和挑战，并提出未来的研究方向和建议，旨在为高尿酸血症肾病的防治提供新的理论依据和实践指导。
