Table 1.

Biomarkers of acute kidney injury

Biomarkers	Source	Clinical significance	Validation	Time of detection	References
Urinary tubular enzymes. Proximal renal tubular epithelial antigen (HRTE-1), α-glutathione S-transferase, pi-glutathione S-transferase, gamma-glutamyltranspeptidase, alanine aminopeptidase, lactate dehydrogenase, N-acetyl-β-glucosaminidase, and alkaline phosphatase	Enzymes Released from damaged tubular epithelial cells	Elevated in AKI and acute tubular necrosis	Further validation is needed to differentiate between prerenal AKI and ATN	It is released within 12 hours of injury and is seen 4 days before the elevation of serum creatinine	Lisowska-MyjakS1
Urinary low-molecular-weight proteins α1-microglobulin, β2-microglobulin, retinol-binding protein, adenosine	Produced at various sites, filtered and reabsorbed by the proximal tubular cells but are not secreted. Increased levels are suggestive of proximal tubular injury or dysfunction	It is presumed that tubular proteinuria indicates the need for kidney replacement therapy in patients with AKI	Further validation is needed	Detected in the urine within 4 hours	Herget-Rosenthal et al.S2
Neutrophil gelatinase-associated lipocalin	Is predominantly produced by thick ascending limb of the loop of Henle and intercalated cells of the collecting duct	Ischemic, septic, post-transplantation AKI, decompensated cirrhosis, type1 cardiorenal syndrome	may be useful for early injury prediction and progression of injury. Can differentiate between ATN vs. prerenal AKI. Approved as biomarker of AKI in some countries	Can be detected 3 hours after injury, peaks in 8–12 hours, persists for 5 days	Albert et al.S3
Urinary kidney injury molecule-1 T cell immunoglobulin mucin domain-1	Produced predominately by proximal tubular epithelial cells in ischemic and toxic injury	Elevated levels correlated with increased risk in death or hospitalization in cardiac studies	Further validation is needed	Detected as early as 24 hours after tubular injury	Ghatanatti et al.S4
Urinary interleukin-18	Formed in the proximal tubules	Biomarker of renal parenhymal injury. Elevated in ATN compared with prerenal AKI, urinary tract infection, or CKD	Further validation is needed	Peaks around 12 hours of injury	Parikh et al.S5
Urinary liver-type fatty acid-binding protein	Secreted by proximal tubular epithelial cells during ischemic and hypoxic injury	Correlates strongly with ischemic time in post-transplant patients, elevated after cardiac surgery, a predictor of poor prognosis	Further validation is needed		Yamamoto et al.S6
Urinary angiotensinogen	is an amino acid cleaved by renin to form angiotensin 1	It is promising to detect progressive AKI, especially in acute decompensated heart failure	Further validation needed		Chen et al.S7
Urinary Calprotectin		Promising role in differentiating ATN vs. prerenal AKI	Further validation neededIt is secreted by immune cells as danger-associated molecular pattern protein	Detected within 2 hours and peaked by 48 hrs	Chen et al.S8
Urinary TIMP-2 × IGFBP-7 (Commercially marketed as NephroCheck)	It induces G1 cell cycle arrest in renal tubular cells to postischemic or septic injury	Predicts AKI in critically ill and perioperative patients	It is approved by US FDA	Detected in the urine within 4 hours whereas serum creatinine took 1 to 3 days to increase	Timi et al.S9

AKI, acute kidney injury; ATN, acute tubular necrosis; CKD, chronic kidney disease; FDA, Food and Drug Administration.