Glomerular nephrotoxicity of aminoglycosides

Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinin...

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Bibliographic Details
Published in:Toxicology and applied pharmacology 2007-08, Vol.223 (1), p.86-98
Main Authors: Martínez-Salgado, Carlos, López-Hernández, Francisco J., López-Novoa, José M.
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Aminoglycosides
Aminoglycosides - adverse effects
Animals
Anti-Bacterial Agents - adverse effects
ANTIBIOTICS
Apoptosis
Apoptosis - drug effects
Biological and medical sciences
CELL PROLIFERATION
CREATININE
GENE REGULATION
Gentamicin
Gentamicins - adverse effects
Glomerular Filtration Rate
Glomerular toxicity
GLOMERULI
Humans
Kidney Diseases - chemically induced
Kidney Diseases - metabolism
Kidney Diseases - pathology
Medical sciences
Mesangial cells
Mesangial Cells - drug effects
Mesangial Cells - pathology
NECROSIS
Platelet-activating factor
Proliferation
REVIEWS
TOXICITY
Toxicology
ULTRAFILTRATION
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Summary:Aminoglycoside antibiotics are the most commonly used antibiotics worldwide in the treatment of Gram-negative bacterial infections. However, aminoglycosides induce nephrotoxicity in 10–20% of therapeutic courses. Aminoglycoside-induced nephrotoxicity is characterized by slow rises in serum creatinine, tubular necrosis and marked decreases in glomerular filtration rate and in the ultrafiltration coefficient. Regulation of the ultrafiltration coefficient depends on the activity of intraglomerular mesangial cells. The mechanisms responsible for tubular nephrotoxicity of aminoglycosides have been intensively reviewed previously, but glomerular toxicity has received less attention. The purpose of this review is to critically assess the published literature regarding the toxic mechanisms of action of aminoglycosides on renal glomeruli and mesangial cells. The main goal of this review is to provide an actualized and mechanistic vision of pathways involved in glomerular toxic effects of aminoglycosides.
ISSN:0041-008X
1096-0333
DOI:10.1016/j.taap.2007.05.004