Gentamicin effects on renal ischemia/reperfusion injury.

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Abstract
Tubular injury. From0-4hoursofreperfusion, gentamicin approximately halved ATP/ADPratios (duetoincreased ADP),indicating a drug-induced defect incellular energetics. Thisabnormality temporally correlated withevolving morpholog- ical damage. Although antioxidants (deferoxamine andsodium benzoate) havebeenreported to protect against pureaminoglycoside nephrotoxicity, theydidnotmitigate gentamicin's adverse impact on postischemic acuterenal failure. Gentamicin didnotinfluence ischemia/immediate reperfusion deacylation/reacylation (assessed byrenal free fatty acidcontent) despite itsknown antiphospholipase activity. Although inthenormalkidney gentamicin preferentially accumu- lated incortex, inthepostischemic kidney, bothcortex andoutermedullary stripe developed striking (approximately threefold tofivefold) andcomparable gentamicin increments. In conclusion, gentamicin appearstoexacerbate postischemic acuterenalfailure byadversely influencing thereperfusion, nottheischemic injury, process.Thismay occurbecause increased gentamicin accumulation negatively impacts on reperfusion cellular energetics. (Circulation Research 1992;70:20-28)