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Nephrotoxicity of several newer agents.

There is widespread agreement that drug nephrotoxicity plays a major role in the high incidence and prevalence of acute renal failure in both hospitalized and nonhospitalized patients. Recent reviews have suggested that between 5% and 10% of acute renal failure recognized in such patients is caused, at least in part, by drugs [2]. Antibiotics play a major role in these nephrotoxicities, but other drugs are clearly implicated in many cases. The incidence of acute renal failure caused by nephrotoxic agents is particularly notable among the elderly, and there are several reasons for this: (1) there is an age-related decline in glomerular filtration rate in older individuals, and this leads to a decreased clearance of primary drugs or the metabolites of such drugs; (2) there may be a decrease in kidney blood flow and an increase in concentration of some drugs in the cells of medulla; (3) primary differences exist between the elderly and nonelderly and pharmacokinetics of drugs. For example, there may be an increase in free-drug concentration in the elderly in conjunction with hypoalbuminemia, or because of retained metabolites [2]; (4) a decrease in total body water may also alter drug distribution in an adverse way; (5) finally, there may also be a decrease in hepatic metabolism with longer half-lives of some drugs. For example, in a recent study by Dowling et al, individuals with underlying renal disease had a decrease in the maximum cytochrome P450 enzyme activity inducible by rifampin as compared to normal controls [3]. With regard to the fate of individuals who develop acute renal failure caused by nephrotoxicity, several outcomes have been reported. In most cases, the drug