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Novel Kidney Biomarkers and Antibiotics-Induced Acute Kidney Injury: A Practical Assessment of Current and Future
Iman Karimzadeh1,2, Sandra L Kane-Gill2,3,4
1Department of Clinical Pharmacy, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Abstract:
Several antibiotics have nephrotoxic potential and an undeniable role in the development of acute kidney injury (AKI). The current AKI definition and operational criteria are dependent on functional biomarkers, serum creatinine and urine output, to identify and quantify kidney dysfunction and injury. However, there is a tremendous amount of research on novel kidney biomarkers that can be used in the assessment (i.e., prediction, detection, and prognosis) of AKI. This narrative review aimed to discuss different aspects of using novel kidney biomarkers in the context of AKI caused by selected anti-infectives including vancomycin, aminoglycosides, amphotericin B, and polymyxins as examples. Clinical studies on biomarker utilization have focused on diagnosis and detection. Urinary tissue inhibitor of metalloproteinases-2/insulin-like growth factor-binding protein-7, urine/plasma neutrophil gelatinase-associated lipocalin, and serum cystatin C are prominent novel kidney biomarkers studied in the milieu of anti-infective-induced AKI. Several practical issues should be considered in the application of novel kidney biomarkers in the context of antibiotic-induced AKI including: (1) the potential impact of non-kidney factors on biomarker results, (2) the utility of an optimal panel of biomarkers, (3) the appropriate starting time, frequency, and time intervals of urine/plasma sampling, (4) having a standard approach for urine sampling (random spot vs. 24-h or serial measurements), (5) ascertainment of clinically significant and diagnostic threshold values/concentrations for each biomarker, and (6) consideration of cost issues for routine use in clinical practice. Overall, novel kidney biomarkers have the potential to improve prediction and detection of antibiotic-induced AKI.
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