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Publication Name World Journal of Nephrology
Manuscript ID 117355
Country India
Category Nutrition & Dietetics
Manuscript Type Editorial
Article Title Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease
Manuscript Source Invited Manuscript
All Author List Pranjal Kashiv, Manish Ramesh Balwani, Amit Pasari, Khushboo Saxena and Vivek B Kute
Funding Agency and Grant Number
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
Key Words Trimethylamine N-oxide; Diabetic kidney disease; Gut microbiota; Renal fibrosis; TGF-β/Smad signalling
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.
Citation Kashiv P, Balwani MR, Pasari A, Saxena K, Kute VB. Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease. World J Nephrol 2026; In press
Received
2025-12-05 00:41
Peer-Review Started
2025-12-05 08:43
First Decision by Editorial Office Director
2026-01-08 08:08
Return for Revision
2026-01-08 08:08
Revised
2026-01-12 09:38
Publication Fee Transferred
Second Decision by Editor
2026-02-02 02:42
Second Decision by Editor-in-Chief
Final Decision by Editorial Office Director
2026-02-03 00:40
Articles in Press
2026-02-03 00:40
Edit the Manuscript by Language Editor
Typeset the Manuscript
ISSN 2220-6124 (online)
Open Access This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Copyright 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.
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