Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Nephrol. Jun 25, 2026; 15(2): 117355
Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.117355
Published online Jun 25, 2026. doi: 10.5527/wjn.v15.i2.117355
Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease
Pranjal Kashiv, Department of Nephrology, All India Institute of Medical Sciences, Nagpur 441108, Mahārāshtra, India
Manish Ramesh Balwani, Department of Nephrology, Saraswati Kidney Care Center, Nagpur 440015, Maharashtra, India
Amit Pasari, Department of Nephrology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Wardha 442001, Mahārāshtra, India
Khushboo Saxena, Department of Nephrology, Institute of Kidney Diseases and Research Center, Ahmedabad 380016, Gujarāt, India
Vivek B Kute, Department of Nephrology, Institute of Kidney Diseases and Research Center, Dr HL Trivedi Institute of Transplantation Sciences, Ahmedabad 380016, Gujarat, India
Author contributions: Kashiv P conceptualized the study, designed the methodology, collected data, performed analysis, and drafted the initial manuscript; Balwani MR and Pasari A provided critical supervision, conceptual guidance, and major revisions of the manuscript; Saxena K assisted in data collection, literature review, and preparation of figures and tables; Kute VB contributed to study design, interpretation of results, and final review of the manuscript for important intellectual content; all authors approved the final version and agree to be accountable for all aspects of the work.
AI contribution statement: AI tools including ChatGPT and Grammarly were used in a limited capacity for language refinement, grammatical correction, and improvement of readability of the manuscript text. ChatGPT was additionally used for limited assistance with image polishing for the purpose of improving visual clarity and presentation quality. No part of the scientific content of the manuscript was generated de novo by AI. All scientific concepts, clinical observations, data interpretations, and conclusions are the original work of the authors. AI tools were used only for linguistic polishing and grammatical correction. They did not contribute to data analysis, study design, translation, or substantive scientific writing. No AI tool participated in the design of the study or in the interpretation of its results. All scientific reasoning was performed entirely by the human authors. No figures or scientific images representing primary data were generated by AI. Any AI-assisted image editing was limited to visual enhancement and did not alter, fabricate, or modify any scientific content of the image. The original image files are available upon request. The authors take full responsibility for the entire content of the manuscript.
Conflict-of-interest statement: All authors declare that they have no conflict of interest to disclose.
Corresponding author: Vivek B Kute, Professor, Department of Nephrology, Institute of Kidney Diseases and Research Center, Dr HL Trivedi Institute of Transplantation Sciences, Civil Hospital Campus, Ahmedabad 380016, Gujarat, India. drvivekkute@rediffmail.com
Received: December 5, 2025
Revised: January 12, 2026
Accepted: February 3, 2026
Published online: June 25, 2026
Processing time: 191 Days and 12.7 Hours
Revised: January 12, 2026
Accepted: February 3, 2026
Published online: June 25, 2026
Processing time: 191 Days and 12.7 Hours
Core Tip
Core Tip: Diabetic kidney disease is increasingly understood as a disorder shaped not only by metabolic and inflammatory injury but also by gut microbial dysbiosis that amplifies renal fibrotic signalling. Song et al demonstrate that trimethylamine N-oxide (TMAO), generated from microbial metabolism of dietary methylamines, functions as a potent upstream driver of transforming growth factor-β/Smad activation and tubulointerstitial fibrosis. Their use of fecal microbiota transplantation and microbial trimethylamine-inhibition provides compelling causal evidence linking dysbiosis, elevated TMAO, and renal injury. This editorial contextualizes these findings within emerging gut-kidney mechanisms and underscores the therapeutic potential of microbiota-targeted strategies in modifying the trajectory of diabetic kidney disease.