Infections caused by multidrug-resistant (MDR) organisms (Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumonia) are major causes of death in critically ill patients. Such patients are inevitably exposed to numerous types of antimicrobial therapies. Colistin is the last resort for these patients. Despite colistin being widely used currently, the drug was previously abandoned due to the significant risk of nephrotoxicity [1]. It has been reintroduced to the market due to a lack of treatment options in such treatment-resistant organisms. The rate of nephrotoxicity differs between studies and has been reported to occur from 10 to 15% [2], to over 50% [3]. and even higher in some studies reaching to 74% [4]. The wide range of frequency of nephrotoxicity probably depends on the definition and the patient characteristics in each of those studies. Obviously, patients with risk factors that may alter kidney function have a higher risk of toxicity [5]. In addition to permanent kidney damage and dialysis dependency, colistin nephrotoxicity increases the risk of mortality [3].

There is no specific recommendation that may indeed prevent colistin nephrotoxicity. Such patients already have an increased risk of kidney failure due to many factors including sepsis, volume alterations, additional nephrotoxic exposures, age, and comorbidities. Colistin brings an enormous additional risk, which is believed to occur via mechanisms related to oxidative stress and apoptosis [1]. Several drugs which work by augmentation of antioxidant pathways could prevent renal damage in animals treated with colistin [6]. Access to an effective treatment that can at least reduce the kidney damage caused by colistin would have a significant effect on patient outcomes. Previous studies have shown benefits from dexmedetomidine when used to reduce kidney damage in the case of ischemia-reperfusion injury [[7], [8], [9], [10], [11], [12]], radiocontrast nephropathy [13], and colistin nephrotoxicity [14,15]. In terms of ischemic protection, dexmedetomidine is known as an alpha-2 adrenoreceptor agonist and has been shown to activate phosphatidylinositol 3-kinase (PI3K-Akt) signaling via α2 adrenoceptors to reduce cell death and plasma high-mobility group protein B1, subsequently inhibiting Toll-like receptor 4 signaling which translates into long-term kidney protection [7]. Dexmedetomidine inhibits secretion of renin and vasopression, and blocks action of vasopression on kidney tubules [14]. Other factors that may explain kidney protective effect of dexmedetomidine may be an increase in renal blood flow [14], and antiinflammatory response [11,16]. Possible nephroprotective effect of dexmedetomidine in critically ill patients receiving colistin has been shown experimentally, yet there is a lack of clinical studies. This observational study aimed to test the possible kidney protective effect of dexmedetomidine in patients under colistin therapy.