Table 1 Emerging pharmacological agents for the treatment of AKI in various models
From: Review on kidney diseases: types, treatment and potential of stem cell therapy
Drugs | Properties |
|---|---|
Teprasiran (QPI 1002) | Teprasiran blocks the expression of p53, which promotes apoptosis [33] |
Levosimendan | levosimendan increases Renal Blood Flow (RBF) through renal vasodilation with preference for the afferent arterioles, resulting in higher intra-glomerular pressure and increased filtration [34] |
Calcitriol [1,25-dihydroxy vitamin D] | Within the proximal tubule of the nephron, the enzyme 1-alpha-hydroxylase transforms calcifediol into calcitriol i.e., the bioactive form of vitamin D which has shown improvement in patients with damaged kidney [32] |
Alkaline phosphatase | Lipopolysaccharide, a pathogen-associated molecular pattern that causes inflammation in sepsis-associated AKI, is detoxified by the endogenous enzyme alkaline phosphatase by dephosphorylation. Moreover, recombinant alkaline phosphate also had a positive impact on long-term renal function [35] |
Nitroglycerin | Nitroglycerin significantly increases the creatinine clearance levels, renal blood flow rate, and serum electrolytes (sodium and potassium) that were disrupted by ischemia–reperfusion. Additionally, it dramatically reduced the effects of a compromised antioxidant defence system and prevented lipid peroxidation [36] |
Furosemide | Furosemide, loop diuretic medicine, working kidney’s helper to remove excess water and electrolyte so being utilised during emergency and when patient in Intensive care unit [37] |