Table 1.
| AKI Biomarker | Biological Role (Source) |
Type of Marker (Sample) |
Time of Increase after Injury | Limitations (Studied Population) |
|---|---|---|---|---|
| Alanine aminopeptidase; alkaline phosphatase; γ-glutamyl transpeptidase | Located in proximal tubular cells; released into urine after tubular damage ([9]) | Damage (urine) | Elevated in UTI, cardiovascular disease, and stroke (patients in the ICU) | |
| Cystatin C | Produced by nucleated human cells; freely filtered ([8,9,10]) | Functional (plasma) | 12–24 h after injury | Confounded by age, sex, inflammatory state, diabetes, low albumin level, muscle mass, and use of high-dose steroids (patients undergoing cardiac surgery or liver transplantation; hospitalized patients) |
| Hepcidin | Predominantly produced in hepatocytes; freely filtered ([10]) | Damage (urine and plasma) | Decreased in anemia and increased in an inflammatory state (patients undergoing cardiac surgery; patients in the ICU) | |
| Tissue metalloproteinase-2; insulin-like growth factor binding protein-7 | Metalloproteinases released during cell-cycle arrest ([8,12,25]) | Stress (urine) | As early as 4 h but typically within 12 h | Elevated in diabetes (patients undergoing cardiac or noncardiac surgery; patients in the ICU; patients in the ED) |
| Interleukin-18 | Released into urine after tubular damage ([9,10]) | Damage (urine) | Elevated in an inflammatory state; lack of cutoff values (hospitalized patients; patients in the ICU or ED; patients undergoing cardiac surgery) | |
| Kidney injury molecule-1 | Produced by proximal tubular cells; released into urine after tubular damage ([8,9,10]) | Damage (urine) | 12–24 h after injury | Elevated in chronic proteinuria and inflammatory diseases (hospitalized patients; patients in the ED; patients undergoing cardiac surgery; patients in the ICU) |
| Liver-type fatty acid-binding protein | Freely filtered and reabsorbed in proximal tubules; released into urine after tubular cell damage ([10]) | Damage (urine and plasma) | Associated with anemia in patients without diabetes (patients undergoing cardiac surgery; patients in the ICU or ED) | |
| N-acetyl-β-D-glucosaminidase | Released into urine after tubular damage ([8,11]) | Damage (urine) | Within 2–4 h after injury | Elevated in diabetes and albuminuria (patients undergoing cardiac surgery; hospitalized patients) |
| Neutrophil gelatinase-associated lipocalin | At least three different types: (1) produced by neutrophils and epithelial tissues, including tubular cells; (2) produced by neutrophils; and (3) produced by tubular cells ([9,10,11]) | Damage (urine and plasma) | Elevated in sepsis, UTI, and CKD; lack of specific cutoff values (patients undergoing cardiac or noncardiac surgery; patients undergoing coronary angiography; patients in the ICU; post-transplantation patients; patients in the ED) | |
| Proenkephalin A | Freely filtered ([26]) | Functional (plasma) | (Patients in the ICU; patients undergoing cardiac surgery; hospitalized patients) |
AKI, acute kidney injury; CKD, chronic kidney disease; ED, emergency department; ICU, intensive care unit; UTI, urinary tract infection.