Table 1.

Novel therapeutic agents for acute kidney injury

Agent	Mechanism of action	Potential indication(s)
Renal blood flow modifiers
Angiotensin	Constricts efferent arterioles to a greater degree than afferent arterioles Regulates release of aldosterone and vasopressin	Sepsis
Adenosine antagonists	Reduces GFR in response to hypoxia Constricts afferent arterioles → increase NaCl levels in proximal tubules	CIN IRI Cardiorenal syndrome
Antioxidants
Alpha-lipoic acid	Reduced form eliminates free radicals Improves glomerular function Reduces renal inflammation	IRI CIN
Selenium	Cofactor that reduces free radicals	Cisplatin injury ECSL
MESNA	Scavenges for free radical oxygen species	CIN
Propofol	Converts free oxygen radicals into a phenoxyl form	IRI
Curcumin	Scavenges for free oxygen radicals Stimulates activity of antioxidant molecules such as superoxide dismutase, catalase, and glutathione peroxidase	IRI Diabetic nephropathy Lupus nephritis
Anti-inflammatory mediators
Alkaline phosphatase	Dephosphorylates lipopolysaccharide Dephosphorylates ATP	Gram-negative sepsis
Dipeptidylpeptidase-4 Inhibitors	Extends half-life of glucagon-like peptide-1	Diabetic nephropathy Cisplatin injury
Sphingosine 1 phosphate (S1P) analogues	Mitigates endothelial damage Decreases recruitment of inflammatory mediators to the renal tubules	None to date
Genetic modifiers
I5NP	Inhibits p53 gene	IRI

ATP, adenosine triphosphate; CIN, contrast induced nephropathy; ECSL, extracorporeal shockwave lithotripsy; GFR, glomerular filtration rate; IRI, ischemia reperfusion injury; MESNA, sodium 2-mercaptoethane sulfonate; NaCl, sodium chloride.