Table 3.

Advantages and disadvantages of novel clinical biomarkers of acute kidney injury

Biomarker	Source	Characteristics	Advantages	Disadvantages
NGAL	Urine Plasma	Ubiquitous epithelial protein Freely filtered by glomerulus, reabsorption at proximal tubule	Increased levels 1–2 hours post-insult 25, 26 Widely investigated in diverse populations 22, 23 Rapid point of care testing available	Decreased specificity in critically ill populations 48
IL-18	Urine	Pro-inflammatory cytokine Injury induced production in proximal tubular epithelial cells	Increased levels 4–6 hours post-insult 60 Widely investigated in diverse populations 41, 46, 58, 59, 61	Increased in general inflammatory conditions 62, 63 Research based testing only
KIM-1	Urine	Membrane glycoprotein expressed in injured proximal tubular epithelial cells Directs phagocytosis of apoptotic cells	Increased specificity for ischemic renal injury 74 Rapid point of care testing reported 72	Delayed increase up to 12 hours post-insult in certain populations 75 Lacking data in the majority of etiologies of acute kidney injury
L-FABP	Urine	Hepatically synthesized cystosolic protein in proximal tubule epithelial cells Limits cell toxicity via sequestration of lipid peroxidation products	Increased levels 4 hours post-insult 6 Baseline levels may prognosticate acute kidney injury 90	May be a non-specific marker of ischemia 91 May be altered in sepsis and liver dysfunction 92 Research based testing only
Cys-C	Urine Plasma	Ubiquitously produced cysteine proteinase inhibitor Freely filtered at glomerulus without secretion or reabsorption Fully catabolized by prox tubule cells, undetectable in normal urine	Increased specificity for proximal tubule dysfunction compared to SCr Rapid clinical testing available	Non-specific marker of GFR suffering similar limitations to SCr Delayed increase up to 8–12 hours post-insult, but more rapid than SCr 100–102 Levels altered by thyroid disease and systemic inflammation 105