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Acute Renal Failure and Toxic Nephropathy

  • Chapter
Contemporary Nephrology

Abstract

Recent prospective studies of hospital-acquired acute renal failure have revealed it to be a serious illness.1,2The development of hospital-acquired acute renal failure is associated with a sixfold increase in risk of dying. In fact, patients who develop an elevation of serum creatinine concentration greater than 3 mg/dl have a mortality rate of 64%. Development of this condition also has a marked impact on the length of stay of a patient in hospital. One recent report demonstrated that the development of acute renal failure increased a patient’s length of stay in the hospital an average of 13–23 days. The most common etiologies of hospital-acquired acute renal failure include aminoglycoside nephrotoxicity, radiocontrast exposure, volume depletion, and septic shock. These etiologies highlight the role of both toxic and ischemic processes in clinically relevant acute renal failure. Prevention of hospital-acquired acute renal failure is, therefore, critically important, not only to diminish the mortality rate associated with this disease process, but also to limit the cost of hospital care. For example, a carefully done retrospective analysis of 1756 patients receiving aminoglycosides was undertaken to determine the economic impact of aminoglycoside associated nephrotoxicity.3 An incidence rate of 7% in these patients was identified for aminoglycoside-associated nephrotoxicity. In this study, the additional cost of treating this complication in these patients totaled approximately $2500 per episode.

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Humes, H.D., Messana, J.M. (1989). Acute Renal Failure and Toxic Nephropathy. In: Klahr, S., Massry, S.G. (eds) Contemporary Nephrology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0829-4_8

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