Table 1.
NGAL | KIM-1 | L-FABP | IL-18 | IGFBP7 and TIMP-2 | Calprotectin | |
---|---|---|---|---|---|---|
Origin | Thick ascending loop of Henle and the intercalated cells of the collecting duct (Schmidt-Ott et al. 2007, Paragas et al. 2014) | Proximal tubule cells (Han et al. 2002, Ichimura et al. 2008) | Proximal tubule cells (Yamamoto et al. 2007) | Collecting duct (Gauer et al. 2007) Tubular epithelial cells (Franke et al. 2012) |
Unknown | Collecting duct and in filtrating immune cells (Fujiu et al. 2011, Seibert et al. 2016) |
Physiological function in the kidney | Bacteriostatic function in the innate immune system, iron delivery to mammalian cells (Goetz et al. 2002, Flo et al. 2004, Bao et al. 2010) | Tubular regeneration by mediating phagocytosis of apoptotic bodies (Ichimura et al. 2008) | Regulation of fatty acids uptake and the intracellular transport (Chmurzyńska 2006) | Proinflammatory effect (Cheung et al. 2005) | Unknown | Polarization of M2 macrophages, promotion of repair after injury (Dessing et al. 2015) |
Animal models | Holo-NGAL protects kidney from damage in response to ischaemia reperfusion injury (Mori et al. 2005) | KIM-1 knockout protects against damage in response to ischaemia reperfusion injury (Ismail et al. 2015b) | Human-L-FABP transgenic mice have less damage after ischaemia and reperfusion (Yamamoto et al. 2007) | IL-18-deficient mice are protected from ischaemia reperfusion-induced AKI (Wu et al. 2008) | Unknown | A lack of active calprotectin leads to more fibrosis after inn response to ischaemia reperfusion injury (Dessing et al. 2015) |
Disadvantages | AKI-independent association with sepsis, CKD, UTI (Devarajan 2007, Schmidt-Ott 2011) | Is induced in various chronic proteinuric, inflammatory diseases (Smith et al. 2006) | Association of L-FABP with anaemia (Imai et al. 2015) | No reliable prediction of AKI | Unclear cellular sources and pathophysiology | Elevated in UTI (Heller et al. 2011) Elevated in urothelial carcinoma (Ebbing et al. 2014) |
Key clinical studies | ||||||
Diagnosis of intrinsic AKI | AUC 0.87 (Singer et al. 2011) AUC 0.81 (Nickolas et al. 2012) AUC 0.95 (Nickolas et al. 2008) |
AUC 0.71 (Nickolas et al. 2012) | AUC 0.70 (Nickolas et al. 2012) | AUC 0.64 (Nickolas et al. 2012) | AUC 0.97 (Heller et al. 2011) AUC 0.99 (Seibert et al. 2013) AUC 0.94 (Seibert et al. 2016) AUC 0.94 (Chang et al. 2015) |
|
Early prediction of AKI | AUC 0.67 (Parikh et al. 2011) AUC 0.72 (Koyner et al. 2010) |
AUC 0.69 (Koyner et al. 2010) AUC 0.71 (Parikh et al. 2013) |
AUC 0.66 (Parikh et al. 2013) AUC 0.69 (Prowle et al. 2015) |
AUC 0.75 (Parikh et al. 2013) AUC 0.55 (Haase et al. 2008) |
AUC 0.85 (Bihorac et al. 2014) AUC 0.80 (Kashani et al. 2013) |
|
Prediction of in-hospital death | Hall et al. (2011), Singer et al. (2011), Nickolas et al. (2012) | Hall et al. (2011), Gonzalez & Vincent (2012), Nickolas et al. (2012) | Doi et al. (2011), Nickolas et al. (2012) | Doi et al. (2011), Hall et al. (2011) | ||
Prediction of long-term ESRD/mortality | Bolignano et al. (2009), Ralib et al. (2012), Coca et al. (2014) | Koyner et al. (2015b) |