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. 2015 Jul;7(2):75–86. doi: 10.5249/jivr.v7i2.615

Table 2. Hallmarks of AKI.

Hallmark * Modulated associated event
RAAS activation ↑ Angiotensin signaling
Na+/Cl- retention, increased luminal Na+ ↑ Aldosterone/cortisol signaling events
Hyperglycemia ↑ Diabetes
Tubular cell dynamics ↑ Infiltration of immature cells
Cytoskeletal reorganization ↑ ECM remodeling
Elevated blood pressure ↑ Hypertension
Accumulation of free and esterified cholesterol ↑ Systemic stress response
PI3K modulation ↓ Phosphoinositol-3-kinase activity
↓ Insulin signaling
Vasoconstriction ↑ Vasoconstrictors (endothelin, angiotensin, MMP2)
↓ Vasodilators (nitric oxide NO)
Hypoxia ↑ Hypoxia inducing factor HIF1α
↑ NADPH oxidases
↑ ROS levels
↑ NFkB activity
↑ Inflammation factors (TNFα, TF, PAT1, MCP1)
↑ Inflammation and inflammatory response
↑ Atherogenesis, fibrinogenesis
↓ ATP levels
↓ NAD levels
↑ Hypoxanthine levels
↑ Necrosis

* Clinical and disease model observations are listed based on modulated associated events, and the arrows represent either up- or down-regulation.