Biomarkers in acute kidney injury
Novel biomarkers such as NGAL, KIM-1, L-FABP, IL-18, cystatin C, and the cell-cycle-arrest pair TIMP-2 and IGFBP7 signal structural kidney injury and can detect acute kidney injury earlier than serum creatinine, serving as adjuncts to improve early diagnosis, differential diagnosis, and prognosis.
Background
Acute kidney injury is diagnosed by changes in serum creatinine and urine output, but these markers reflect function rather than injury and rise only after substantial damage has occurred, with significant time delay. This limitation has driven the search for biomarkers that derive from the injured kidney and reflect molecular processes intimately connected with tissue injury, enabling earlier and more precise detection.
Key recommendations
The most studied AKI biomarkers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and calprotectin, alongside the filtration marker cystatin C. These molecules localize to specific nephron segments and reflect distinct pathophysiological processes including tubular injury, inflammation, and repair, allowing them to be used as adjuncts to creatinine and urine output for early detection and risk stratification.
Clinical implications
Used together with conventional markers, these biomarkers can improve early diagnosis, differentiate kidney injury from dysfunction, identify subclinical AKI, and provide prognostic information including risk of dialysis, progression to chronic kidney disease, and death. However, each biomarker has advantages and limitations, performance varies with assay thresholds and timing, and important knowledge gaps remain regarding tissue correlation and optimal clinical integration.
Category
News
Source
Annals of Intensive Care
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