Aminoglycoside antibiotics are employed clinically because of their potent bactericidal activities, less bacterial resistance, post-antibiotic effects and low cost. However, drugs belong to this class are well-known to cause nephrotoxicity, which limits their frequent clinical exploitation. Gentamicin, a commonly used aminoglycoside, is associated with an induction of tubular necrosis, epithelial oedema of proximal tubules, cellular desquamation, tubular fibrosis, glomerular congestion, perivascular edema and inflammation, which ultimately show the way to renal dysfunction. It is a matter of debate whether we have promising agents to prevent the incidence of gentamicin-induced nephrotoxicity. The present review critically discussed the pathogenesis of gentamicin-induced nephrotoxicity. In addition, based on the experimental and clinical studies, the possible therapeutic approach to prevent gentamicin-induced nephrotoxicity has been discussed.
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Article Synopsis
- * Thirty male Wistar rats were used in the experiment, divided into groups receiving either gentamicin, beta-carotene, both, or control treatments, with tests done on serum and tissues to evaluate hepatorenal function.
- * Results showed that beta-carotene significantly reduced markers of liver and kidney damage (like SGOT, SGPT, creatinine, and urea levels) compared to gentamicin alone, suggesting it may be beneficial as an additional treatment for patients receiving gentamicin.
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