Acute Kidney Injury (AKI)
Mechanism of action
Acute Kidney Injury (AKI) is a severe inflammation and damage of the kidney resulting in a sudden drop in kidney function, which can sometimes result in complete kidney failure. AM-Pharma has discovered that one key function of the enzyme Alkaline Phosphatase (AP) is to protect organs against inflammation and tissue damage.
AP acts as a detoxifying agent by removing phosphate from extracellular substrates. The dephosphorylation of pro-inflammatory substances like lipopolysaccharides (LPS) and extracellular ATP plays an important anti-inflammatory role. Research has shown that ATP dephosphorylation has a double effect in protecting against kidney injury. When the pro-inflammatory ATP is dephosphorylated the resulting adenosine further reduces inflammation through the activation of the immunosuppressive adenosine A2a receptor pathway (A2aR).
Our proprietary recombinant human AP (recAP) has a dual mechanism of action via dephosphorylation of lipopolysaccharides (LPS) and extracellular ATP. We have shown that treatment of patients with exogenous AP not only reduces local and systemic inflammation but also protects the kidney against further damage.
The anti-inflammatory properties of AP were first published by professor Poelstra and team at Groningen University, the Netherlands. Our scientists and affiliated researchers have since published extensively on the role of AP in AKI. Read more in our publication section.
For further information on the mode of action of AP in AKI patients please see: