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已发表论文
尿酸肾病中的肠-肾轴：微生物群、代谢交互作用及转化前景
Authors Liang J, Qiu Y, Fu T, Li J, Yang J, Tong Y
Received 16 October 2025
Accepted for publication 9 December 2025
Published 18 December 2025 Volume 2025:18 Pages 8111—8132
DOI https://doi.org/10.2147/JMDH.S574758
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Charles V Pollack
Jiahao Liang,1 Yanzhi Qiu,1 Tong Fu,2 Jianing Li,1 Jiamin Yang,1 Ying Tong1
1Graduate School, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, 150040, People’s Republic of China; 2Department of Psychology, Brandeis University, Waltham, MA, 02453, USA
Correspondence: Ying Tong, Graduate School, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, 150040, People’s Republic of China, Email tongying@hljucm.edu.cn
Abstract: Uric acid nephropathy (UAN) represents a critical and multifactorial renal disorder closely linked to hyperuricemia, inflammation, and gut microbiota dysregulation. Recent advances have revealed the pivotal role of the gut–kidney axis in modulating urate metabolism, immune activation, and oxidative stress. This review synthesizes emerging preclinical and clinical evidence to construct an integrative framework for understanding UAN, highlighting both crystal-dependent and crystal-independent mechanisms that drive tubular injury and fibrosis. Accumulating data underscore the reciprocal crosstalk between renal dysfunction and gut dysbiosis, mediated by microbial metabolites such as short-chain fatty acids (SCFAs), indoxyl sulfate, and p-cresol sulfate. We further evaluate therapeutic interventions targeting the gut–kidney axis—including probiotics, synbiotics, postbiotics, fecal microbiota transplantation (FMT), and engineered microbial therapies—which have shown promise in restoring microbial balance and improving urate handling. By integrating multi-omics profiling with systems biology, this review proposes a precision-medicine roadmap that leverages microbiome signatures and metabolic phenotyping for risk stratification and personalized intervention. Moreover, we emphasize the need for supportive regulatory frameworks and interdisciplinary collaboration to enable the clinical translation of microbiota-based strategies. Collectively, this work provides a strengthened conceptual foundation for microbiome-informed prevention and treatment of uric acid–related kidney disease.
Keywords: uric acid nephropathy, hyperuricemia, gut–kidney axis, microbiota, inflammation, oxidative stress, probiotics
1Graduate School, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, 150040, People’s Republic of China; 2Department of Psychology, Brandeis University, Waltham, MA, 02453, USA
Correspondence: Ying Tong, Graduate School, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, 150040, People’s Republic of China, Email tongying@hljucm.edu.cn
Abstract: Uric acid nephropathy (UAN) represents a critical and multifactorial renal disorder closely linked to hyperuricemia, inflammation, and gut microbiota dysregulation. Recent advances have revealed the pivotal role of the gut–kidney axis in modulating urate metabolism, immune activation, and oxidative stress. This review synthesizes emerging preclinical and clinical evidence to construct an integrative framework for understanding UAN, highlighting both crystal-dependent and crystal-independent mechanisms that drive tubular injury and fibrosis. Accumulating data underscore the reciprocal crosstalk between renal dysfunction and gut dysbiosis, mediated by microbial metabolites such as short-chain fatty acids (SCFAs), indoxyl sulfate, and p-cresol sulfate. We further evaluate therapeutic interventions targeting the gut–kidney axis—including probiotics, synbiotics, postbiotics, fecal microbiota transplantation (FMT), and engineered microbial therapies—which have shown promise in restoring microbial balance and improving urate handling. By integrating multi-omics profiling with systems biology, this review proposes a precision-medicine roadmap that leverages microbiome signatures and metabolic phenotyping for risk stratification and personalized intervention. Moreover, we emphasize the need for supportive regulatory frameworks and interdisciplinary collaboration to enable the clinical translation of microbiota-based strategies. Collectively, this work provides a strengthened conceptual foundation for microbiome-informed prevention and treatment of uric acid–related kidney disease.
Keywords: uric acid nephropathy, hyperuricemia, gut–kidney axis, microbiota, inflammation, oxidative stress, probiotics