RESUMEN
The purpose of the present investigation was to examine the effects of two nonsteroidal anti-inflammatory drugs [NSAIDs], ibuprofen [20 mg/kg/day] and diclofenac sodium [2.5 mg/kg/day], on the severity of gentamicin - induced nephrotoxicity in rats. Administration of gentamicin [100 mg/kg/day] for 5 days resulted in a significant elevation in renal cortical total phospholipids accompanied by a significant decrease in cortical Na[ +/- ] K[ +/- ] adenosine triphosphatase [ATPase] activity [P<0.01]. These changes were associated with significant decrease in body weight and increase in kidney weight. Serum creatinine and urea nitrogen were also elevated in all gentamicin treated rats [P<0.01]. In rats treated simultaneously with both gentamicin and either ibuprofen or diclefenac sodium for 5 days, all the measured parameters of renal dysfunction were similar in magnitude to those observed in rats treated with gentamicin alone. In contrast, rats treated with either ibuprofen or diclofenac sodium for 27 days and injected concurrently with gentamicin during the last 5 days of the treatment period had significantly greater kidney weight, lower renal cortical Na[ +/- ]K[ +/- ] ATPase activity and higher cortical phospholipid content, serum creatinine and urea nitrogen than did rats treated with gentamicin alone [P<0.05]. A 27 -day treatment with ibuprofen or diclofenac sodium alone resulted in no change in renal function. These results demonstrate that gentamicin nephrotoxicity was potentiated after the long [27 days] but not after the short [5 days] period of treatment with ibuprofen and diclofenac sodium. Thus, prolonged administration of NSAIDs even in therapeutic doses should be considered as a risk/actor that may increase the nephrotoxic potential of gentamicin