Abstract
To assess whether PAF could be involved in the gentamicin-induced nephrotoxicity, we have studied the effect of PAF antagonist BN-52021 on renal function in rats after gentamicin (GENTA) treatment. Experiments were completed in 21 Wistar rats divided into three groups: group GENTA was injected with gentamicin 100 mg kg−1 body wt/day s.c. for 6 days. Group GENTA + BN received gentamicin and BN-52021 i.p. 5 mg kg−1 body wt/day. A third group served as control. Rats were placed in meta-bolic cages and plasma creatinine and creatinine clearance were measured daily. GENTA group showed a progressive increase in plasma creatinine, a drop in creatinine clearance and an increase in urinary excretion of N-acetyl-β-D-glucosaminidase and alkaline phosphatase. GENTA + BN group showed a lesser change in plasma creatinine and a creatinine clearance, but no difference with GENTA group in urinary excretion of NAG and AP were observed. Histological examination revealed a massive cortical tubular necrosis in rats treated with gentamicin, whereas in BN-52021 injected animals tubular damage was markedly attenuated. The present results suggest a role for PAF in the gentamicininduced nephro-toxicity.
Highlights
Gentamicin is an aminoglycoside frequently used in the treatment of gram-negative infection
Platelet activating factor (PAF) has been shown to be produced by the kidney5’6 and to be involved in the reduction of glomerular filtration rate (GFR) observed in experimental models of acute renal failure (ARF). 7’8 To assess whether PAF could be involved in the gentamicin-induced nephrotoxicity, we have studied in rats after gentamicin treatment, the effect on renal function and morphology of inhibiting the interaction of PAF with its receptor using a specific antagonist of PAF, BN-52021
Rats treated with gentamicin and BN-52021 showed a lower increase in plasma creatinine and a lower decrease in creatinine clearance (Figs 1 and 2)
Summary
Gentamicin is an aminoglycoside frequently used in the treatment of gram-negative infection. Gentamicin-induced nephrotoxicity is mainly tubular, and cellular necrosis confined to cells of the nephron segment where gentamicin is absorbed, chronic treatment with gentamicin has been reported to induce decreases in glomerular filtration rate (GFR).4 7’8 To assess whether PAF could be involved in the gentamicin-induced nephrotoxicity, we have studied in rats after gentamicin treatment, the effect on renal function and morphology of inhibiting the interaction of PAF with its receptor using a specific antagonist of PAF, BN-52021.
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