12 For these reasons, there is a broad consensus amongst the clinical and basic AKI research communities that development of the first effective disease modifying treatments for AKI will address an important, unmet medical need. 11 In a 2018 report by MarketWatch, the number of AKI patients in 2016 was estimated to be over 1.5M with the market size being $4.3B in the seven major markets including the US, EU5 (Germany, Spain, Italy, France, and UK), and Japan. 5– 8 In terms of the scale of the problems, AKI has been reported to complicate up to 20% of hospitalizations 9, 10 with a prevalence rate estimated to be 1.8 in 1000 in the general population in a 2007 study. Currently, no therapeutic interventions have been shown to definitively prevent AKI, improve recovery, or improve long-term outcomes after AKI, including CKD, ESRD or death. 2– 4 Despite the clinical significance of this problem, supportive care, avoiding additional kidney injury, and when possible, removing the initial injurious event, are the primary treatment options. 2– 4 AKI from any cause is a strong, independent predictor of mortality, and often results in incomplete recovery, giving rise to CKD, and in some patients, end stage renal disease (ESRD). 2– 4 AKI also commonly occurs in association with comorbidities including pre-existing chronic kidney disease (CKD), old age, diabetes and heart failure, all of which increase the risk of AKI and may influence the underlying pathobiology and response to treatment. 1– 3 Despite this simple and homogeneous definition, AKI is in fact a highly heterogeneous clinical syndrome that is precipitated by different injurious events, often in combination, including dehydration, heart failure, blood loss, major trauma including surgery and crush injury, sepsis and chemical toxicities. This review will examine and make the case that CO be developed into a therapeutic agent against AKI.Īcute kidney injury (AKI) is a common, global health concern that manifests as a rapid decline in kidney function that occurs over a 7-day period or less. This is particularly important in treating cisplatin-induced AKI, a common clinical problem that develops in patients receiving cisplatin therapies for a number of different solid organ malignancies. CO has also been shown to sensitize cancer, but not normal cells, to chemotherapy. Along this line, carbon monoxide (CO) has emerged as a promising therapeutic agent because of its demonstrated cytoprotective, and immunomodulatory effects. However, over the same time period, new understanding of the underlying pathobiology and molecular mechanisms of kidney injury have undoubtedly helped the search for new therapeutics. Over the years, there has been much effort in search of therapeutics with minimal success. There is also a large untapped market opportunity in treating AKI. Treating acute kidney injury (AKI) represents an important unmet medical need both in terms of the seriousness of this medical problem and the number of patients.
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