Table 3.
Name (Abbreviation) | Known Inciting Factors | Proposed Functional Role in AKI |
---|---|---|
Neutrophil gelatinase–associated lipocalin (NGAL) | Ischemia, toxin | Protective: apoptosis inhibition |
Kidney injury molecule 1 (KIM-1) | Ischemia-reperfusion | Protective: promotes removal of apoptotic and necrotic products |
Interleukin 18 | Ischemia-reperfusion, toxin | Proinjury: inflammatory cytokine |
Liver-type fatty acid–binding protein (L-FABP) | Ischemia, cardiac surgery | Protective: antioxidant |
Angiotensinogen (Atg) | Cardiac surgery, others | Proinjury: RAAS activation |
Tissue inhibitor of metalloproteinase-2 (TIMP-2) | Cardiac surgery, critical illness | Protective: unclear mechanisms |
Insulin like growth factor binding protein 7 (IGFBP-7) | Critical illness | Protective: cell-cycle arrest |
AKI, acute kidney injury; RAAS, renin-angiotensin-aldosterone system.
Alge and Arthur.78