Abstract
Acute kidney injury is a common complication in critically ill patients with sepsis and/or septic shock. Further, some essential antimicrobial treatment drugs are themselves nephrotoxic. For this reason, timely diagnosis and adequate therapeutic management are paramount. Of potential acute kidney injury (AKI) biomarkers, non-protein-coding RNAs are a subject of ongoing research. This review covers the pathophysiology of vancomycin and gentamicin nephrotoxicity in particular, septic AKI and the microRNAs involved in the pathophysiology of both syndromes. PubMED, UptoDate, MEDLINE and Cochrane databases were searched, using the terms: biomarkers, acute kidney injury, antibiotic nephrotoxicity, sepsis, miRNA and nephrotoxicity. A comprehensive review describing pathophysiology and potential biomarkers of septic and toxic acute kidney injury in septic patients was conducted. In addition, five miRNAs: miR-15a-5p, miR-192-5p, miR-155-5p, miR-486-5p and miR-423-5p specific to septic and toxic acute kidney injury in septic patients, treated by nephrotoxic antibiotic agents (vancomycin and gentamicin) were identified. However, while these are at the stage of clinical testing, preclinical and clinical trials are needed before they can be considered useful biomarkers or therapeutic targets of AKI in the context of antibiotic nephrotoxicity or septic injury.
Highlights
Acute kidney injury (AKI) is a common and mostly severe clinical syndrome complicating a number of critical illnesses
Renal impairment and serum creatinine levels that had not returned to baseline levels by 90 days resulted in the need for renal replacement therapy (RRT) and/or progression to chronic kidney disease (CKD) [2]
This review focuses on the pathophysiology and potential biomarkers in the detection of AKI after nephrotoxic drugs and/or septic insults with emphasis on specific microRNAs
Summary
Acute kidney injury (AKI) is a common and mostly severe clinical syndrome complicating a number of critical illnesses. It has a highly negative impact on patient morbidity, mortality and clinical outcome. According to the KDIGO (Kidney Disease Improving Global Outcomes) classification of 2012, the severity of urinary output deterioration to terminal stages and presentation of an anuria and serum creatinine increase to 353.6 μmol/L is the most serious stage 3 [1]. AKI diagnosis, especially in critically ill patients, would enable clinicians to better initiate preventive measures to avoid the need for RRT and obviate the risk of CKD. This review focuses on the pathophysiology and potential biomarkers in the detection of AKI after nephrotoxic drugs and/or septic insults with emphasis on specific microRNAs
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