Acute kidney injury due to gentamicin nephrotoxicity and specific miRNAs as biomarkers.

Autor:	Klementa V; Department of Internal Medicine III - Nephrology, Rheumatology and Endocrinology, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic., Petejova N; Faculty of Medicine, Palacky University Olomouc, Czech Republic.; Department of Internal Medicine and Cardiology, University Hospital Ostrava, Czech Republic.; Faculty of Medicine, University of Ostrava, Czech Republic., Horak P; Department of Internal Medicine III - Nephrology, Rheumatology and Endocrinology, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic., Kurasova E; Department of Internal Medicine III - Nephrology, Rheumatology and Endocrinology, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic., Zadrazil J; Department of Internal Medicine III - Nephrology, Rheumatology and Endocrinology, Faculty of Medicine and Dentistry, Palacky University Olomouc and University Hospital, Olomouc, Czech Republic.
Jazyk:	angličtina
Zdroj:	Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia [Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub] 2024 Oct 11. Date of Electronic Publication: 2024 Oct 11.
DOI:	10.5507/bp.2024.031
Abstrakt:	Acute kidney injury (AKI) due to gentamicin nephrotoxicity is a significant concern in clinical medicine, particularly in patients receiving prolonged or high-dose gentamicin therapy. Gentamicin is an aminoglycoside antibiotic frequently used in the treatment of a range of bacterial infections. However, its use is associated with nephrotoxicity which can manifest as AKI. Due to this, it is crucial to diagnose promptly and manage treatment effectively. Ongoing studies are therefore focusing on non-protein-coding RNAs as potential biomarkers for AKI. Numerous microRNAs (miRNAs) have been implicated in gentamicin-induced nephrotoxicity and AKI. They participate in pathways associated with inflammation, cell death, and oxidative stress and each of these factors play critical roles in the development of gentamicin-induced kidney injury. Research studies have demonstrated changes in the expression levels of these miRNAs in response to gentamicin exposure both in vitro and in in vivo models, as well as in human clinical trials involving patients receiving gentamicin therapy. The dysregulation of these miRNAs correlates with the severity of kidney injury and may serve as sensitive biomarkers for early detection and monitoring of AKI induced by gentamicin. Competing Interests: The authors report no conflicts of interest in this work.
Databáze:	MEDLINE
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