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Acute kidney injury (AKI) is a critical condition with diverse manifestations and variable outcomes. Its diagnosis traditionally relies on delayed indicators such as serum creatinine and urine output, making early detection challenging. Early identification is essential to improving patient outcomes, driving the need for novel biomarkers. Recent advancements have identified promising biomarkers across various biological processes. Tubular injury markers, including neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), N-acetyl-β-D-glucosaminidase (NAG), and liver-type fatty acid-binding protein (L-FABP), offer insights into early tubular damage. Inflammatory and repair-associated biomarkers, such as interleukin-18 (IL-18), monocyte chemotactic protein-1 (MCP-1), osteopontin (OPN), and C-C motif chemokine ligand 14 (CCL14), reflect ongoing injury and recovery processes. Additionally, stress and repair markers like tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor-binding protein-7 (IGFBP-7), alongside filtration markers such as cystatin C (CysC) and proenkephalin (PenKid®) e.tal, further enhance diagnostic precision. Oxidative stress-related markers, including Superoxide Dismutase 1 (SOD1), also contribute valuable information. Emerging candidates, such as microRNAs, soluble urokinase plasminogen activator receptor (SuPAR), and chitinase-3-like protein 1 (CHI3L1), hold substantial promise for AKI detection and prognosis. This review summarizes the progress in AKI biomarker research, highlighting their clinical utility and exploring their potential to refine early diagnosis and management strategies. These findings offer a new perspective for integrating novel biomarkers into routine clinical practice, ultimately improving AKI care.
Yang et al. (Wed,) studied this question.