Novel Drugs for Acute Kidney Injury

Abstract Acute kidney injury (AKI) is a complex disease, but understanding is lacking regarding the pathophysiology on a molecular basis. Treatment has been largely supportive, including volume management, avoidance of nephrotoxins, hemodynamic management, and renal replacement therapy. Recent data have emerged that implicate fluid overload and chloride in the development of acute kidney injury. A conservative fluid management strategy with a balanced, buffered solution is an emerging tactic in the fight against AKI. New efforts aimed at looking deeper into the causes of acute kidney injury have focused on inflammation, immune dysregulation, and oxidative injury. New targets have been correlated to certain types of kidney injury, such as metalloproteinase, which are reflective of cellular dysfunction. Others include intermedin, adenosine, inducible nitric oxide synthase, vitamin D, and sphingosine 1 phosphate, which are implicated in inflammation, apoptosis, and oxidative damage. Novel candidate therapies include direct oxygen free radical scavengers such as ALA, curcumin, I5NP, MESNA, propofol, and selenium, which act as direct oxygen free radical scavengers. Angiotensin II and adenosine receptor antagonists may ameliorate kidney injury via manipulation of renal hemodynamics and tubule-glomerular feedback. S1P analogues, alkaline phosphatase and DPP-4 inhibitors counteract kidney injury via manipulation of inflammatory pathways.