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Exp Nephrol. 1997 Jan-Feb;5(1):47-54.

Involvement of platelet-activating factor in gentamicin nephrotoxicity in rats.

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Instituto Reina Sofia de Investigacion Nefrologica, Departamento de Fisiologia y Farmacologia, Universidad de Salamanca, Espana.


To assess whether platelet-activating factor (PAF) could be involved in gentamicin-induced nephrotoxicity, we studied the effect of PAF antagonist BN-52021 on renal function in rats after gentamicin treatment. Administration of gentamicin resulted in a progressive increase of plasma creatinine, a drop in creatinine clearance and an increase of urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and alkaline phosphatase (AP). Rats treated with BN-52021 and injected with gentamicin showed fewer changes in plasma creatinine and creatinine clearance, but no differences in urinary excretion of NAG and AP were observed in gentamicin-treated rats. Histological examination revealed massive cortical tubular necrosis in rats treated with gentamicin, whereas in BN-5202 1-injected animals tubular damage was markedly attenuated. Glomeruli from gentamicin-treated rats produced larger amounts of PAF than glomeruli from control rats. In addition, in the group of BN-52021- and gentamicin-treated rats, glomerular PAF production was not significantly different from that of the control group. The present results suggest a role for PAF in gentamicin-induced nephrotoxicity.

[Indexed for MEDLINE]

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