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Letter to the Editor
©Author(s) (or their employer(s)) 2026. No commercial re-use. See Permissions. Published by Baishideng Publishing Group Inc.
World J Crit Care Med. Mar 9, 2026; 15(1): 114998
Published online Mar 9, 2026. doi: 10.5492/wjccm.v15.i1.114998
Revisiting acute kidney injury outcomes in traumatic brain injury
Nupur Karan, Rohit Patnaik
Nupur Karan, Department of Anaesthesiology, All India Institute of Medical Sciences, Raipur 492099, Chhattisgarh, India
Rohit Patnaik, Department of Critical Care Medicine, Medeor 24x7 Hospital, Abu Dhabi 40330, United Arab Emirates
Author contributions: Karan N wrote the original draft; Karan N and Patnaik R contributed to the conceptualization, writing, reviewing, and editing, participated in drafting the manuscript; all authors have read and approved the final version of the manuscript.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Corresponding author: Rohit Patnaik, DM, Department of Critical Care Medicine, Medeor 24x7 Hospital, Al Falah Street – Al Danah – Zone 1, Abu Dhabi 40330, United Arab Emirates. rohitpatnaik09@gmail.com
Received: October 9, 2025
Revised: November 21, 2025
Accepted: January 9, 2026
Published online: March 9, 2026
Processing time: 143 Days and 17.5 Hours
Abstract

Acute kidney injury in traumatic brain injury is a major concern, affecting up to 10% of the patients in intensive care unit due to multifaceted mechanisms, including hemorrhagic shock, rhabdomyolysis, and brain-kidney cross-talk, compounded by hyperosmolar therapies. A significant challenge is that serum creatinine is considered a late and nonspecific marker, often missing the critical early insult phase. Future strategies for early prediction and prevention must focus on emerging factors, such as preventing hyperchloremia and utilizing novel biomarkers, such as neutrophil gelatinase-associated lipocalin and kidney injury molecule 1, which detect subclinical injury and predict the need for renal replacement therapy. Composite risk stratification tools (e.g., renal angina index) are vital for personalized management. Although over 90% of patients recover renal function, prevention of collateral damage to the kidney must be recognized as a critical priority in traumatic brain injury care.

Keywords: Trauma-related acute kidney injury; Traumatic brain injury; Brain-kidney crosstalk; Neutrophil gelatinase-associated lipocalin; Biomarkers; Renal replacement therapy; Hyperchloremia; Risk-stratification

Core Tip: Trauma-related acute kidney injury is a critical concern in traumatic brain injury care, affecting up to 10% of intensive care unit patients. Since creatinine is a late marker, early prediction is vital. Strategies must focus on preventing hyperchloremia using novel biomarkers (e.g., neutrophil gelatinase-associated lipocalin/kidney injury molecule 1) and risk stratification tools to detect subclinical injury and prevent collateral kidney damage.