The high incidence of associated nephrotoxicity represents an important concern in the use of aminoglycoside antibiotics, which have been implicated as one of the primary causes of drug-induced acute renal failure. Several factors, including the underlying health of the patient, criteria used to define nephrotoxicity, and the specific aminoglycoside administered, may contribute to the nephrotoxic potential of these agents. The development of aminoglycoside-induced nephrotoxicity is a complex problem. These drugs appear to be only minimally metabolized within the body and undergo nearly exclusive renal excretion, primarily by glomerular filtration. Ultimately, reabsorption and accumulation within the kidney results in proximal tubular cell damage; several possible mechanisms have been proposed, both for the development of such cell damage and for its subsequent role in the evolution of nephrotoxicity. The pathology and the clinical pattern of aminoglycoside-induced kidney damage have been extensively studied in animal models and in humans. Although the data often conflict, many of these studies have attempted to identify some of the factors associated with a higher risk for aminoglycoside nephrotoxicity. Of the factors generally agreed upon to influence risk, correction of volume depletion and diminished renal perfusion, as well as dose adjustment for level of renal function, have been identified as critical measures for prevention of renal damage by aminoglycosides. Recent studies have indicated that newer agents, such as third-generation cephalosporins and aztreonam, often may be as therapeutic and cost-effective as the aminoglycosides without the nephrotoxicity associated with the latter agents.(ABSTRACT TRUNCATED AT 250 WORDS)