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The Landscape of Biomarkers in ICU-Associated AKI: From Protein Markers to Cell-Free Nucleic Acids
Qi Zhu1, Feng Yang2, Hua Zheng3
1Department of Emergency, Central Hospital Affiliated to Shenyang Medical College, Shenyang, China.
Background:
Acute kidney injury (AKI) affects approximately 30%-60% of intensive care unit (ICU) admissions, but early detection remains difficult because creatinine- and urine-output-based KDIGO criteria are delayed and confounded in critical illness.
Objective:
To summarize the biomarker landscape for ICU-associated AKI, focusing on kidney-targeted injury/stress proteins and circulating cell-free DNA (cfDNA), including mitochondrial DNA (mtDNA).
Methods:
PubMed/MEDLINE and Embase were searched from inception to December 31, 2025, using terms related to AKI, critical illness, NGAL, KIM-1, IL-18, L-FABP, [TIMP-2]·[IGFBP7], cfDNA, mtDNA, and damage-associated molecular patterns. Adult ICU studies reporting diagnostic performance, risk stratification, or clinically relevant outcomes were prioritized, especially in sepsis, cardiac surgery, shock, and trauma.
Results:
NGAL, KIM-1, IL-18, L-FABP, and [TIMP-2]·[IGFBP7] often rise before creatinine or urine-output changes, providing early kidney-proximal signals of tubular injury or stress. cfDNA/mtDNA instead reflects systemic cell death, mitochondrial damage, and innate immune activation, capturing multi-organ injury and adding prognostic information beyond clinical scores and creatinine. Across ICU phenotypes, combining clinical risk, an early kidney-targeted marker, and cfDNA/mtDNA may improve identification of patients at risk for severe AKI, renal replacement therapy, and death.
Conclusions:
Multimarker strategies may widen the diagnostic window and sharpen prognostication in ICU-associated AKI. Routine implementation will require standardized pre-analytical handling, assay harmonization, biomarker-guided pragmatic trials, and trajectory-based decision tools that demonstrate clinical benefit.
